Epidemic encephalitis B, commonly referred to as Japanese encephalitis, is an acute pestilence of the central nervous system caused by the Japanese encephalitis virus and transmitted by mosquitoes. It predominantly occurs during the summer and autumn seasons and is most commonly seen in children under the age of 10.

bubble_chart Clinical Manifestations

In the first 1–2 days of illness, there is only fever, and after 2–3 days, the fever becomes higher, possibly accompanied by headache, fatigue, drowsiness, nausea, vomiting, and grade I neck stiffness. Based on the progression of the condition, it can be divided into the following 4 types.

1. Mild type: The body temperature is around , the patient is conscious, without convulsions, with grade I headache, nausea, vomiting, and drowsiness, and no obvious meningeal irritation signs. The course of the illness lasts 5–7 days.
2. Moderate type (common type): There is impaired consciousness such as lethargy or light unconsciousness, meningeal irritation signs, disappearance of abdominal wall reflexes and cremasteric reflexes, and occasional short-term convulsions. The body temperature rises to 39–40°C, the course lasts 7–10 days, and there are no sequelae.
3. Severe type: The child has persistent high fever above 40°C, unconsciousness, repeated or continuous convulsions, obvious meningeal irritation signs and increased intracranial pressure, disappearance or hyperactivity of deep and superficial reflexes, and positive pathological reflexes. The course lasts more than 2 weeks, and a few children may have sequelae.
4. Fulminant type: The body temperature suddenly rises above 41°C, and the child quickly falls into deep unconsciousness with continuous convulsions. Cerebral edema, brain herniation, and respiratory failure may occur, and most children die within 3–5 days. Survivors may have severe sequelae. Severe or fulminant types are more common in the early stages of an epidemic, while mild types are more prevalent in the late stage [third stage] of the epidemic.

bubble_chart Auxiliary Examination

1. The blood routine mainly shows leukocytosis, ranging from 10 to 30×10⁹/L, with neutrophils accounting for 70–90%.
2. The cerebrospinal fluid appears colorless, transparent, or slightly turbid, with normal or slightly elevated pressure. The cell count increases to 50–500×10^6/L, predominantly neutrophils in the first 2–5 days of illness, followed by lymphocytes. Protein grade I is elevated, glucose is slightly increased or normal, and chloride levels are normal. Within 1–2 weeks of onset, the activity of aspartate aminotransferase (AST) in the cerebrospinal fluid may increase.
3. Serological tests: (1) Complement fixation test: Antibody titers rise significantly 3–5 weeks after onset. A fourfold or greater increase in antibody titers between paired sera (acute and convalescent phases, one month apart) confirms the diagnosis. A single serum titer of 1:2 is suspicious, and 1:4 is positive. (2) Hemagglutination inhibition test: Antibodies appear early, and a fourfold or greater increase in paired serum titers confirms the diagnosis. A single serum titer of 1:160 is suspicious, and 1:320 is positive. (3) Specific antibody (IgM) testing: Antibodies appear as early as 4 days after illness onset, aiding early diagnosis, peaking at two weeks. (4) PCR detection of Japanese encephalitis virus DNA is positive.

bubble_chart Diagnosis

Epidemiological history: The disease has a strict seasonal pattern, predominantly occurring in July, August, and September. Incidence rates are higher in regions with high temperatures, heavy rainfall, and abundant mosquito populations.

bubble_chart Treatment Measures

﹝Treatment﹞

(1) General Treatment Patients should be hospitalized. After admission, closely observe changes in consciousness, monitor body temperature, pulse, respiration, and blood pressure. Continuously monitor pupil size. Once changes occur, symptomatic treatment should be administered promptly. Pay attention to nutrition and calorie supplementation; unconscious patients may be given nasal feeding. For patients with frequent spasms, intravenous fluids should be administered at a daily volume of 50–0 ml/kg. When using dehydrating agents, ensure potassium salts are supplemented. Unconscious patients should be turned frequently to keep the skin clean and dry, preventing bedsores. Maintain oral hygiene. For unconscious patients who cannot close their eyes, protect the eyes by ensuring cleanliness and safeguarding the cornea. For children with convulsions, prevent tongue biting and ensure the tongue does not fall back to obstruct the airway. (2) Symptomatic Treatment

1. For high fever, lower the room temperature (controlled at 26–28°C). Administer physical cooling measures such as alcohol sponge baths, lukewarm baths, or ice packs. Analgin may be administered nasally or Bupleurum intramuscularly. For persistent high fever or convulsions, sub-hibernation therapy may be used (with chlorpromazine and promethazine, 0.5–1 mg/kg each, administered intramuscularly every 4–6 hours).
2. To control convulsions, antispasmodics can be used, such as phenobarbital sodium at 5–8 mg/(kg·dose) intramuscularly; diazepam at 0.1–0.3 mg/(kg·dose) intramuscularly or intravenously, but it should not be administered immediately after phenobarbital to prevent respiratory depression; chloral hydrate at 40 mg/(kg·dose) for retention enema; and paraldehyde at 0.15–0.2 ml/(kg·dose) intramuscularly, with a maximum dose not exceeding 5 ml. Each of these antispasmodics can be administered every 4–6 hours and used alternately. Additionally, if convulsions are caused by cerebral edema, dehydration therapy should be administered; if caused by hypoxia due to blocked respiratory secretions or insufficient ventilation, suction and oxygen therapy should be provided, and tracheostomy with assisted ventilation may be necessary during seasonal epidemics; if caused by high fever, antipyretic treatment should be given. 3. Management of respiratory failure: First, analyze the cause of respiratory failure and implement rescue measures. Ensure airway patency and provide oxygen. For respiratory failure caused by brain parenchymal inflammation, cerebral edema, or brain herniation, dehydrating agents, corticosteroids, and respiratory stimulants may be used. (1) Maintain airway patency and clear mucus blockages. Thoroughly suction secretions as needed, turn the patient regularly, and perform back patting. For thick secretions, 0.5% chymotrypsin at 0.1 mg/kg with appropriate antibiotics can be administered via nebulization, along with nasal oxygen. Tracheostomy and even assisted ventilation may be performed for patients with frequent convulsions and risk of asphyxia, those with excessive and difficult-to-clear secretions, those confirmed by blood gas analysis to have respiratory failure, or those with concurrent pneumonia. (2) Central respiratory stimulants: These are more effective when used before spontaneous respiration ceases. Lobeline at 0.15–0.2 mg/kg per dose, nikethamide at 5–12.5 mg/kg per dose, and dimefline at 2–6 mg per dose can be alternated and repeated every 4–6 hours if necessary. Note that excessive doses may induce convulsions. (3) Dehydrating agents: These should be administered immediately for children with intracranial hypertension or cerebral edema. Commonly used dehydrating agents include 20% mannitol at 1.0–2.0 g/kg per dose, 25% sorbitol at 1.0–2.0 g/kg per dose, 30% urea at 0.5–1.0 g/kg per dose, and furosemide at 1 mg/kg per dose. These should be infused within 15 minutes to 1 hour or given intravenously if necessary. Administer every 4–6 hours for a course of 3–5 days. Monitor for electrolyte imbalances, with fluid intake at about 70% of the required volume to maintain mild dehydration. Be cautious of rebound phenomena after discontinuation. (4) Corticosteroids: These can be used early in severe cases or when the condition is unpredictable. Administer hydrocortisone intravenously at 5 mg/(kg·dose) or dexamethasone at 2.5–5–10 mg/(kg·dose), with a general course not exceeding 5–7 days. (3) Antibiotics: Appropriate antibiotics should be selected for concurrent bacterial infections. (4) Immunotherapy: This helps reduce mortality, with treatment courses lasting 3–7 days. 1

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TCM's treatment of atopic dermatitis is more comprehensive, fundamental, non-toxic and effective than Western medicine's symptomatic treatment

1. Drugs that promote functional recovery, such as ATP, coenzyme A, cytochrome C, and γ-aminobutyric acid. Additionally, vitamins B
   1. B12, etc.
2. For symptomatic treatment of tremor and increased muscle tone, Artane can be taken at 1–2 mg per dose, 2–3 times daily.
3. Tuina, physical therapy, and functional training can provide some assistance in the recovery of limb paralysis and aphasia.

bubble_chart Prevention

(1) Vaccination Complete the vaccination with inactivated Japanese encephalitis vaccine one month before the annual epidemic season. After the first initial dose, a second dose should be administered 7 to 10 days later. Subsequently, one dose should be given annually. Immunity lasts for one year, with a protection rate of 80–90%. (2) Controlling the Source of Infection Isolate patients until their body temperature returns to normal. Vaccinating susceptible animals (such as pigs) before the epidemic season can reduce the incidence rate. (3) Mosquito Elimination and Prevention Eliminate mosquito breeding grounds. Unprocessed Rehmannia Root.

bubble_chart Differentiation

It should be differentiated from toxic dysentery, purulent meningitis, subcutaneous nodular meningitis, poliomyelitis, viral encephalitis, and malignant malaria (cerebral type).