| disease | Purulent Meningitis |
| alias | Brain, Purulent Meningitis |
Purulent meningitis (abbreviated as purulent meningitis) is an inflammation of the meninges caused by various pyogenic bacterial infections. It is common in children, especially infants. Since the use of antibiotics, its mortality rate has decreased from 50-90% to less than 10%, but it remains one of the serious infectious diseases in children. Among them, meningococcal meningitis is the most common and can occur in epidemics, with unique clinical manifestations, known as epidemic cerebrospinal meningitis.
bubble_chart Epidemiology
In China, Streptococcus pneumoniae is the most common cause, followed by Haemophilus influenzae. However, in Europe and the United States, the proportion of Haemophilus influenzae meningitis is higher, which may be related to differences in bacterial populations, immune status of the population, and the sensitivity of testing methods. In China, Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae account for more than two-thirds of pediatric bacterial meningitis cases. Newborns are prone to Gram-negative enteric bacilli meningitis, with Escherichia coli being the most common, followed by Proteus, Pseudomonas aeruginosa, and Aerobacter. Group B β-hemolytic streptococcus is more common abroad. Staphylococcus aureus meningitis is often caused by sepsis or may complicate infections due to trauma, surgery, or congenital malformations.
Bacteria can reach the brain membrane through various pathways, such as direct inoculation via trauma or surgery, or dissemination through the lymphatic system or bloodstream. Typically, meningitis develops from bacteremia. Bacteria often invade from the upper respiratory tract, initially hiding and multiplying in the nasopharynx before entering the bloodstream. They then directly reach the blood vessels supplying the central nervous system or form local thrombi there, releasing bacterial emboli into the circulation. Because children's defense and immune functions are weaker than those of adults, pathogens can more easily cross the blood-brain barrier to reach the brain membrane, leading to bacterial meningitis. The skin, mucous membranes, gastrointestinal tract of infants and young children, as well as the umbilical region of newborns, are also common entry points for infection. Sinusitis, otitis media, and mastoiditis can harbor bacteria as infection sites or directly spread to the brain membrane due to disease progression.
bubble_chart Pathological ChangesThe lesions are primarily in the central nervous system. In early and mild cases, inflammatory exudates are mostly on the surface of the cerebral cortex, gradually spreading to cover the entire brain surface, base, and spinal cord with a layer of pus. The subarachnoid space is filled with seropurulent secretions, especially in front of the pons, the floor of the fourth ventricle, and between the pons and cerebellum. The blood vessels on the surface of the meninges are severely congested, often accompanied by vasculitis, including thrombosis of blood vessels and sinuses, necrosis, rupture, and hemorrhage of the vessel walls.
bubble_chart Clinical Manifestations
The clinical manifestations of bacterial meningitis caused by various bacteria are generally similar and can be summarized as infection, increased intracranial pressure, and meningeal irritation symptoms. The clinical presentation largely depends on the age of the child. Older children exhibit symptoms similar to adults, while infants and young children often have more subtle or atypical symptoms.
In childhood, bacterial meningitis has an acute onset, with symptoms such as high fever, headache, vomiting, loss of appetite, and lethargy. At the onset, consciousness is usually clear, but as the condition progresses, drowsiness, delirium, convulsions, and unconsciousness may occur. In severe cases, convulsions and unconsciousness may appear within 24 hours. Physical examination often reveals impaired consciousness, delirium, or unconsciousness, neck stiffness, and positive Kernig's and Brudzinski's signs. If untreated, neck stiffness worsens, leading to head retraction, back muscle rigidity, and even opisthotonos. Irregular breathing patterns and abnormal respiration, accompanied by pupillary changes, indicate severe cerebral edema and impending brain herniation. Herpes is commonly seen in the late stage of meningococcal meningitis [third stage], but it may also occasionally occur in pneumococcal or Haemophilus influenzae meningitis.
In infants and young children, the onset of bacterial meningitis can vary in speed. Due to the unfused anterior fontanelle and open cranial sutures, symptoms of increased intracranial pressure and meningeal irritation may appear later, making the clinical presentation atypical. It often begins with irritability, dysphoria, restlessness, pale complexion, and reduced appetite, followed by fever and respiratory or digestive symptoms such as vomiting, diarrhea, or mild cough. Subsequently, drowsiness, head retraction, hyperesthesia, high-pitched crying, vacant stare, or fixed gaze may occur, sometimes accompanied by head-hitting or head-shaking. Parents often only seek medical attention after convulsions develop. A bulging anterior fontanelle and positive Brudzinski's sign are important indicators, and sometimes a positive skin scratch test may be observed.Neonates, especially premature infants, exhibit markedly different clinical manifestations. The onset is insidious, often lacking typical symptoms and signs. Rare intrauterine infections may present as irreversible shock or apnea at birth, leading to rapid death. More commonly, the infant appears normal at birth but develops hypotonia, reduced movement, weak crying, poor sucking, refusal to feed, vomiting, jaundice, cyanosis, and irregular respiration—non-specific symptoms. Fever may or may not be present, or the body temperature may even drop. Physical examination may only reveal increased anterior fontanelle tension, with few other meningeal irritation signs. Bulging of the anterior fontanelle also appears late, making misdiagnosis highly likely. Only a lumbar puncture to examine cerebrospinal fluid can confirm the diagnosis.
bubble_chart Auxiliary Examination1. Blood Picture: The total white blood cell count and neutrophils are significantly increased. Anemia is commonly seen in Haemophilus influenzae meningitis.
2. Blood Culture: Positive results can be obtained in early stages or in cases not treated with antibiotics, which helps identify the pathogenic bacteria.
3. Throat Culture: Isolating pathogenic bacteria has reference value.
4. Petechial Smear: In children with meningococcal meningitis, the positive rate of bacterial detection in skin petechial smears can exceed 50%.
5. Cerebrospinal Fluid (CSF) shows typical purulent changes. It appears turbid or like thin rice water, with increased pressure. Microscopic examination reveals a high white blood cell count, reaching hundreds of millions/L, with sugar levels often below 150mg/L. Sugar quantification not only helps distinguish bacterial from viral infections but also reflects treatment efficacy. Protein qualitative tests are mostly strongly positive, with quantities usually above 1g/L. Centrifuging and staining the CSF sediment often reveals pathogenic bacteria, providing a basis for early antibiotic selection.
6. Using immunological techniques to detect bacterial antigens in the CSF, blood, or urine of patients is a specific method for rapid pathogen identification, with CSF antigen detection being the most critical.
(1) Counter-Immunoelectrophoresis (CIE): This method uses known antibodies (specific antisera) to detect antigens in CSF (e.g., soluble capsular polysaccharides). It has high specificity and is commonly used for rapid diagnosis of meningococcal meningitis, as well as for detecting Haemophilus influenzae and Streptococcus pneumoniae, with a positive rate of 70–80%.
(2) Detection results for meningococci and Haemophilus influenzae are similar to those obtained by CIE. However, sensitivity for Streptococcus pneumoniae is lower. This method is more sensitive than CIE but may yield false positives.
(3) Fluorescent-labeled known antibodies are added to the test antigen (e.g., CSF or blood samples), and antigen-antibody reactions are observed under a fluorescence microscope. This method is highly specific and sensitive, enabling rapid diagnosis, but requires specialized equipment.
(4) Enzyme-Linked Immunosorbent Assay (ELISA).
(5) Limulus Amebocyte Lysate Test.
7. (1) Normal CSF contains very low levels of immunoglobulins, with IgM absent. In children with purulent meningitis, IgM levels are significantly elevated; if above 30mg/L, viral infection can largely be ruled out.
(2) Normal CSF LDH averages: Newborns 53.1 IU; Infants 32.6 IU; Toddlers 29.2 IU; School-age children 28.8 IU. Normal LDH isoenzyme values: Newborns—LDH127%, LDH235%, LDH334%, LDH243%, LDH51%. After one month of age—LDH137%, LDH232%, LDH328%, LDH42%, LDH51%. In children with purulent meningitis, LDH levels are markedly elevated, with significant rises in LDH4 and LDH5.
(3) The average normal CSF lactate level is 159mg/L. Bacterial meningitis exceeds 200mg/L, while aseptic meningitis is above 250mg/L. A CSF lactate level >350mg/L is diagnostic for bacterial meningitis, with no false positives or negatives. Low lactate levels often rule out purulent meningitis.
Due to the varying pathogenic microorganisms, clinical courses, treatment methods, and prognoses of different types of meningitis, the first clinical step is to distinguish whether it is purulent meningitis and to identify the bacterial species. Many central nervous system infections present with clinical manifestations similar to purulent meningitis, making it impossible to diagnose purulent meningitis based solely on symptoms and general physical examination. It is essential to pay attention to the patient's gaze and the tension of the anterior fontanelle (some infants may have a less full anterior fontanelle due to dehydration, but it remains tense). For suspected cases, a lumbar puncture should be performed early to examine the cerebrospinal fluid for further confirmation. Only during the epidemic season of meningococcal meningitis, when the child exhibits typical symptoms and petechiae, and the clinical diagnosis is already clear, can the cerebrospinal fluid examination be omitted. The possibility of purulent meningitis should be considered under the following circumstances: ① The child has respiratory or other infections such as upper respiratory infection, pneumonia, otitis media, mastoiditis, osteomyelitis, cellulitis, or sepsis, accompanied by neurological symptoms. ② The child has congenital defects such as scalp or midline spinal sinus abnormalities or head trauma, accompanied by neurological symptoms. ③ Infants with unexplained persistent fever that does not respond to general treatment. ④ Young children with high fever and convulsions that cannot be explained by typical febrile seizures. In early neonatal meningitis, the pathogens have just begun to invade the meninges, and changes in the cerebrospinal fluid may not be obvious. If suspicion remains high, the examination should be repeated after one or two days. If the child exhibits severe headache, frequent vomiting, convulsions, elevated blood pressure, optic disc edema, or other signs of increased intracranial pressure, the decision to perform a lumbar puncture should be made with extreme caution. To prevent brain herniation, mannitol (1g/kg) can be administered intravenously to reduce intracranial pressure beforehand. Half an hour later, a lumbar puncture with a stylet-equipped needle can be performed, and the child should remain lying flat for at least two hours afterward.
Identifying the pathogenic bacteria is crucial for effective treatment. Although preliminary assumptions about the causative bacteria can be made based on age, season, and other epidemiological data, as well as the clinical course, further confirmation relies on cerebrospinal fluid smear, bacterial culture, and antigen detection methods such as counterimmunoelectrophoresis.
The onset of this disease is generally acute. The cerebrospinal fluid appears slightly turbid or grade I cloudy, with a slight increase in white blood cells, but later dominated by mononuclear cells. Protein levels are grade I elevated, while glucose and chloride levels remain normal. Attention should be paid to epidemiological characteristics and unique clinical manifestations to aid differentiation. In some viral infections, the total cell count in the cerebrospinal fluid may significantly increase, with polymorphonuclear leukocytes predominating. However, glucose levels are usually normal, and cerebrospinal fluid IgM, lactate dehydrogenase, and its isoenzymes (LDH4, LDH5) do not increase, which can help differentiate.
The onset is often gradual, usually preceded by 1–2 weeks of general malaise. However, abrupt onset can occur, especially in infants with miliary tuberculosis. In typical tuberculous meningitis, the cerebrospinal fluid appears ground-glass-like and may sometimes appear yellow due to high protein content. The white blood cell count ranges from 200–300×106/L, occasionally exceeding 1000×106/L, with mononuclear cells accounting for 70–80%. Glucose and chloride levels are significantly reduced. Protein levels increase to 1–3g/L, and acid-fast bacilli can be found in the cerebrospinal fluid membrane smear. A thorough history of tuberculosis exposure should be taken, and other body parts should be examined for tuberculosis lesions. Tuberculin tests and searches for tuberculosis bacteria in sputum and gastric fluid can aid diagnosis.
The clinical manifestations, course, and cerebrospinal fluid changes resemble those of tuberculous meningitis, but the onset is slower and more insidious, with a longer and fluctuating course. Diagnosis is confirmed by identifying thick-capsuled, shiny round fungal bodies in the cerebrospinal fluid using India ink staining and the growth of Cryptococcus neoformans on Sabouraud's medium.
However, brain abscesses generally have a slower onset, sometimes with localized symptoms. Cerebrospinal fluid pressure is significantly elevated, with normal or slightly increased cell counts and mildly elevated protein levels. When a brain abscess ruptures into the subarachnoid space or ventricles, it can cause typical purulent meningitis. Further confirmation can be achieved through cranial ultrasound, CT, or MRI scans.
The disease course is prolonged and more insidious, generally presenting with signs of increased intracranial pressure and may include abnormal focal neurological signs, often lacking manifestations of infection. Differentiation mainly relies on CT and MRI examinations.
It is a cerebral symptom reaction caused by acute infection and toxins, mostly due to cerebral edema rather than the direct action of pathogens on the central nervous system, thus differing from central nervous system infections. Its clinical features include delirium, spasm, and unconsciousness, and may present with meningeal irritation symptoms or cerebral paralysis. Cerebrospinal fluid only shows increased pressure with no other significant changes.
Mollaret's meningitis is rare and characterized by benign recurrence. For details, see pneumococcal meningitis.
bubble_chart Treatment Measures
1. The prognosis of purulent meningitis is closely related to whether the pathogen is identified early and appropriate antibiotics are selected for treatment. After a preliminary diagnosis through cerebrospinal fluid examination, appropriate and sufficient antibiotics should be administered intravenously as soon as possible, preferably bactericidal drugs. The full course of treatment should be completed as planned according to the condition, without reducing the drug dose or changing the administration method. Failure to identify the pathogen is often due to inappropriate antibiotic use before the diagnosis is confirmed. During the epidemic season of meningococcal meningitis, older children should generally first consider meningococcus as the cause, and the presence of petechiae or ecchymosis makes it even more suspicious. Penicillin, ampicillin, or sulfonamides can be used initially, and the medication can be adjusted based on the response. For sporadic cases with an undetermined pathogen, especially in infants and young children, treatment should initially follow the protocol for purulent meningitis with an unknown pathogen, and the medication can be changed once the pathogen is identified. Currently, third-generation cephalosporins such as ceftriaxone or cefotaxime, or second-generation cephalosporins such as cefuroxime, are often recommended.
When the treatment effect is satisfactory, the fever usually subsides within about 3 days, symptoms improve, bacteria disappear from the cerebrospinal fluid, and the cell count significantly decreases. Other generation and transformation indicators also show corresponding improvement. At this point, the original medication can be continued, and a follow-up cerebrospinal fluid examination should be performed after two weeks. If the treatment response is poor, a timely lumbar puncture should be performed to observe changes in the cerebrospinal fluid, determine whether the medication used is appropriate, and adjust the treatment plan accordingly.
Given that purulent meningitis is a severe central nervous system infection with a prognosis closely tied to treatment, the criteria for discontinuing medication should be strictly followed. These include the disappearance of symptoms, being fever-free for over a week, a cerebrospinal fluid cell count of less than 20×106/L (all mononuclear cells), and normal protein and glucose levels (the criteria for discontinuing medication for meningococcal meningitis are discussed in another section). Generally, achieving these standards fully requires at least 8–10 days, sometimes over a month, with an average of about 2–3 weeks.
(1) The age of the child provides some guidance for antibiotic selection. For example, older children are less likely to have Haemophilus influenzae meningitis, while neonatal purulent meningitis is mostly caused by Gram-negative enteric bacilli. Generally, aminoglycosides combined with penicillin are recommended, as gentamicin and amikacin are effective against Gram-negative enteric bacilli, while penicillin is effective against streptococci, pneumococci, and meningococci. Ampicillin, a broad-spectrum antibiotic, can also be used instead of penicillin. For resistant strains, ampicillin plus cefotaxime can be used. Chloramphenicol is generally contraindicated in neonates, especially premature infants, due to their immature liver and kidney function, which impairs the metabolism and excretion of chloramphenicol, leading to toxicity manifested as "gray baby syndrome" or even shock and death.
(2) Ensuring effective drug concentration in the cerebrospinal fluid: First, drugs that easily cross the blood-brain barrier should be selected to achieve antibiotic concentrations in the cerebrospinal fluid that are at least 10 times the inhibitory concentration. The administration method and dose should also be carefully considered. Chloramphenicol, sulfadiazine, and intravenous trimethoprim (TMP) can reach the cerebrospinal fluid effectively and maintain antibacterial concentrations, especially chloramphenicol, which also crosses inflamed meninges more readily. As the meningeal permeability gradually normalizes with improvement, the amount of drug entering the cerebrospinal fluid decreases. To ensure therapeutic efficacy, high-dose intravenous administration should be maintained until the end of the course, without reducing the dose or changing the administration method midway.
Erythromycin, carbenicillin, vancomycin, first- and second-generation cephalosporins, and aminoglycoside antibiotics have poor ability to cross the blood-brain barrier.
(3) If the selected drug can effectively cross the blood-brain barrier, intrathecal injection is generally unnecessary to avoid adverse reactions and reduce the child's suffering. Drugs such as gentamicin and amikacin do not easily reach the cerebrospinal fluid (CSF), so intrathecal or intraventricular administration may be used. For infants with advanced-stage bacterial meningitis who have delayed diagnosis and treatment, CSF with visible pus formation, or bacterial resistance to antibiotics, adding intrathecal antibiotic injections can improve the cure rate. Depending on the duration of the antibiotic's presence in the CSF, injections are given daily or every other day, typically for 3–5 consecutive times, until the CSF becomes clear, the cell count significantly decreases, and bacteria disappear. If Staphylococcus or rare bacteria are present, or if the CSF still shows significant inflammatory changes after 3–5 intrathecal injections, the duration of intrathecal injections may be extended, even up to 7–10 consecutive times. During intrathecal injection, the drug must be diluted to a certain concentration, either with withdrawn CSF or saline. Note that the volume of injected fluid should be slightly less than the volume of CSF withdrawn, and the injection speed should be slow.
(4) Intraventricular drug administration: Due to the blood-brain barrier and unidirectional cerebrospinal fluid circulation, intravenous and intrathecal injections are ineffective for children with concurrent ventriculitis, as drugs struggle to reach the ventricles. The antibiotic concentration in ventricular fluid also rarely reaches 50 times the minimum inhibitory concentration. Therefore, recent approaches advocate intraventricular drug administration to enhance efficacy. For children with significantly increased intracranial pressure or hydrocephalus, lateral ventricular puncture is used for drug delivery, combined with controlled cerebrospinal fluid drainage for decompression.
2. Except for meningococcal meningitis, conventional use of hydrocortisone was previously recommended after confirming the diagnosis of bacterial meningitis, switching to oral prednisone after 2–5 days for 10–20 days to reduce intracranial inflammatory adhesions. Although adrenal corticosteroids have no direct therapeutic effect on bacterial meningitis, their use was believed to aid fever reduction and alleviate symptoms like intracranial hypertension and infection toxicity. However, rigorous controlled studies have shown no significant impact on reducing mortality or sequelae.
3. Symptomatic management: Certain symptoms or complications can directly threaten a child’s life and require prompt intervention.
(1) Controlling seizures: Frequent seizures must be managed to prevent cerebral hypoxia and respiratory failure, often caused by intracranial hypertension or hypocalcemia. Besides using dehydrating agents to reduce intracranial pressure and routine calcium supplementation, anticonvulsant drugs like diazepam, chloral hydrate, paraldehyde, and phenobarbital are essential.
(2) Reducing intracranial pressure.
(3) Managing shock and DIC.
(4) After diagnosis, a slow infusion of 3% saline at 6ml/kg can increase blood sodium by 5mmol/L. If correction is insufficient, an additional 3–6ml/kg may be given. Fluid intake should be restricted to 800–900ml/m 2 daily, with the composition matching standard maintenance fluids. Due to excessive sodium use, potassium and calcium loss must be compensated.
(5) Large fluid collections (e.g., abdominal mass) can elevate intracranial pressure, compress brain tissue, and worsen long-term outcomes. Since effusions are often infection-related and sometimes purulent, they rarely resolve without drainage. Puncture drainage should be considered under these conditions: ① Positive transillumination warrants puncture to determine fluid nature. ② Small, non-purulent effusions with low protein and no intracranial hypertension may resolve spontaneously in 1–2 months with monitoring. ③ Subdural empyema with significant inflammatory changes, high protein, yellow fluid, or intracranial hypertension requires drainage. Initial punctures (daily or every other day) should remove <30ml per side (≤60ml total). Frequency can be reduced over 1–2 weeks as symptoms improve. ④ For refractory effusions with persistent intracranial hypertension or focal deficits, surgical membrane removal was historically advised to prevent brain atrophy or neurological sequelae, though recent decades lack such reports. Conservative observation often leads to spontaneous resolution. ⑤ For subdural empyema, local irrigation with antibiotics (dose referencing intrathecal injection) and dexamethasone (1mg/dose) may be administered.
4. The ward should be well-ventilated with suitable temperature. For children in the acute phase, close monitoring is required, including regular measurement of respiration, pulse, blood pressure, observation of urine output, respiratory status, and pupil changes, to detect shock and brain herniation early. During the acute phase of bacterial meningitis, the fluid intake for children should be controlled at 1000–1200 ml/(2·d), which is 75% of the normal physiological requirement. It is essential to ensure adequate intake while avoiding excessive fluid infusion that may exacerbate cerebral edema. For those with concurrent dehydration, fluid replacement should be based on the deficit volume; otherwise, cerebral perfusion may be compromised.
Factors related to the prognosis of purulent meningitis include: the age of the child, the type of infecting bacteria, the severity of the condition, the timing of treatment, the presence of complications, and the sensitivity of the bacteria to antibiotics. Infants and young children have poor resistance, making early diagnosis difficult and resulting in a poor prognosis. The mortality rate of neonatal purulent meningitis can reach 65–75%, especially in cases of intrauterine infection with enteric bacteria, which has an extremely poor prognosis. Cases caused by Staphylococcus aureus or enteric bacteria have high mortality rates due to bacterial resistance and treatment difficulties. The mortality rate of purulent meningitis caused by Streptococcus pneumoniae can reach 15–25%, and it is prone to relapse and recurrence.
Purulent meningitis, especially pneumococcal meningitis, mostly develops from upper respiratory tract infections. Therefore, it is essential to pay close attention to respiratory infections in infants. Establishing a good daily routine, keeping warm, getting plenty of sunlight, breathing fresh air, and engaging in necessary outdoor activities can help strengthen the body's resistance. Additionally, minimizing contact with individuals suffering from respiratory infections is crucial to preventing such infections. This is particularly important for reducing the recurrence of pneumococcal meningitis. The prevention of neonatal meningitis is related to perinatal care, and maternal infections should be thoroughly treated. If newborns are exposed to heavily contaminated environments, prophylactic antibiotics should be administered.
1. If the fluid in the subdural space exceeds 2ml, with a protein quantification above 0.4g/L and red blood cells below 1 million × 106/L, it can be diagnosed as subdural effusion.
2. Acute diffuse cerebral edema leading to increased intracranial pressure is a common complication. If severe and rapidly progressing, it may result in temporal lobe herniation or occipital bone foramen magnum herniation. Lack of awareness and failure to promptly adopt dehydration therapy for timely rescue can be life-threatening. Special attention is required for children with intracranial hypertension during transfer; osmotic diuretics should be administered first to reduce pressure, and transfer should only occur after the condition stabilizes. Since the anterior fontanelle and sutures in infants are not yet closed, they can compensate, so the manifestations of increased intracranial pressure are often atypical, and the incidence of brain herniation is relatively lower compared to older children.
3. This is an important cause of poor prognosis and severe sequelae, particularly common in cases caused by Gram-negative bacilli. The infection spreads via the bloodstream, direct extension through choroid membrane fissures, or retrograde diffusion through cerebrospinal fluid. ① Positive results from bacterial culture or smear of ventricular fluid, often consistent with lumbar puncture fluid findings. ② Ventricular fluid white blood cell count ≥ 50 × 106/L, predominantly polymorphonuclear cells. ③ Ventricular fluid glucose < 300mg/L or protein quantification > 400mg/L. ④ Inflammatory changes in ventricular fluid (e.g., increased cell count, elevated protein, reduced glucose) are more pronounced than in lumbar puncture cerebrospinal fluid. Among these four criteria, the first alone can serve as a definitive diagnostic condition. The second criterion requires one of the third or fourth criteria for confirmation.
4. In meningitis, purulent exudate can easily block narrow passages or cause adhesions, leading to cerebrospinal circulation disorders and resulting in hydrocephalus. This is commonly seen in patients with improper or delayed treatment, especially in newborns and young infants. Adhesive arachnoiditis often occurs at the occipital bone foramen magnum, obstructing cerebrospinal fluid flow, or ventricular membrane inflammation causing adhesions, both of which are common causes of obstructive hydrocephalus.
5. Children with purulent meningitis may experience water and electrolyte imbalances due to vomiting or irregular feeding, as well as cerebral hyponatremia, presenting with symptoms such as lethargy, convulsions, unconsciousness, edema, generalized weakness, reduced muscle tone in limbs, and oliguria. This is related to infection affecting the posterior pituitary, leading to excessive antidiuretic hormone secretion and water retention.
6. Damage to brain parenchyma and adhesions can involve cranial nerves or cause limb paralysis, and may also lead to brain abscess, intracranial stirred pulse inflammation, or secondary epilepsy. Fulminant meningococcal meningitis may be complicated by DIC and shock. Additionally, otitis media, pneumonia, and arthritis may occasionally occur.
1. The onset of this disease is generally acute, with the cerebrospinal fluid appearing slightly turbid or grade I cloudy. The white blood cell count ranges from a dozen to several hundred per milliliter, with a slight increase in polymorphonuclear cells in the early stage, but later mononuclear cells predominate. Protein is grade I elevated, while sugar and chloride levels are normal. Attention should be paid to epidemiological characteristics and specific clinical manifestations to aid in differentiation. In the early stages of certain viral encephalitis, especially enterovirus infections, the total number of cells in the cerebrospinal fluid may significantly increase, with polymorphonuclear leukocytes predominating. However, the sugar level is generally normal, and the absence of elevated cerebrospinal fluid IgM, lactate dehydrogenase, and its isoenzymes (LDH4, LDH5) can help differentiate.
2. The onset is usually slow, often preceded by 1–2 weeks of general malaise. However, some cases may present abruptly, especially in infants with miliary subcutaneous node. In typical subcutaneous node meningitis, the cerebrospinal fluid appears ground-glass-like and sometimes yellowish due to high protein content. The white blood cell count is 200–300×106/L, occasionally exceeding 1000×106/L, with mononuclear cells accounting for 70–80%. Sugar and chloride levels are significantly reduced. Protein increases to 1–3 g/L, and acid-fast bacilli can be found in cerebrospinal fluid membrane smears. A thorough inquiry into the patient’s exposure to subcutaneous node, examination for subcutaneous node lesions in other body parts, subcutaneous node bacillus tests, and searches for subcutaneous node bacilli in sputum and gastric fluid can aid diagnosis. For highly suspected cases that are difficult to confirm, anti-tuberculosis drugs should be administered to observe treatment response.
3. Its clinical manifestations, course, and cerebrospinal fluid changes resemble subcutaneous node meningitis, but the onset is slower and more insidious, the course is longer, and symptoms may fluctuate and worsen. Diagnosis relies on identifying thick-capsule, shiny round fungal bodies in cerebrospinal fluid India ink staining and the growth of Cryptococcus neoformans on Sabouraud’s medium.
4. However, brain abscesses generally have a slower onset, sometimes with focal symptoms. Cerebrospinal fluid pressure is significantly elevated, cell counts are normal or slightly increased, and protein is slightly elevated. When a brain abscess ruptures into the subarachnoid space or ventricle, it can cause typical purulent meningitis. Further confirmation can be aided by cranial B-ultrasound, CT, or MRI.
5. The course is longer and more insidious, usually presenting with signs of intracranial hypertension and abnormal local neurological signs, often lacking infection symptoms. Differentiation mostly relies on CT or MRI.
6. This is a general cerebral symptom reaction caused by acute infection and toxins, mostly due to brain edema rather than direct pathogen effects on the central nervous system, thus differing from central nervous system infections. Clinical features include delirium, spasms, unconsciousness, and possible meningeal irritation or cerebral paralysis. Cerebrospinal fluid shows only elevated pressure with no other significant changes.
7. Mollaret’s meningitis—rare, characterized by benign recurrence. For details, refer to pneumococcal meningitis.
