Collection
zero Useful+1
zero

Japanese encephalitis

Announce Upload video
Japanese encephalitis
This entry is made by Good Doctor Online Provide content and participate in editing.
Zhang Yunzhou (Deputy Chief Physician) Intensive Care Unit, Department of Neurology, Xuanwu Hospital, Capital Medical University
Su Yingying (Chief physician) Intensive Care Unit, Department of Neurology, Xuanwu Hospital, Capital Medical University
Japanese B encephalitis (JAPANESE B ENCEPHALITIS) is caused by JE virus infection. The pathogen was first found in Japan in 1934, so it is called Japanese encephalitis B. In 1939, Japanese encephalitis virus was also isolated in China. After liberation, a lot of investigation and research work was carried out. In 1952, it was uniformly named as epidemic encephalitis B, or simply Japanese encephalitis, commonly known as encephalitis, and listed as a legal infectious disease. Clinically, high fever Consciousness obstacle , convulsion respiratory failure It is characterized by symptoms and signs such as meningeal irritation, with a high case fatality rate of about 25%. JE is spread by mosquito vectors, mainly in summer and autumn. Children are vulnerable to JE, and the incidence rate is more than 80%, mostly children under 10 years old. It is popular throughout Asia, mainly in tropical, subtropical and temperate countries in eastern Asia.
Western medicine name
Japanese encephalitis
Department
Internal Medicine - Neurology Department
Common location
cerebral
Common causes
JE virus infection

Disease classification

Announce
edit
According to the severity of the disease, it can be divided into four types:

light

Consciousness to mild lethargy, appearing Meningeal irritation sign ​、 fever Or convulsions in case of high fever.

Normal

Drowsiness or shallow coma, extensive meninges and brain parenchyma involvement. This type is the most common, and light and ordinary types account for about 2/3 of patients with JE.

heavy

Coma, frequent convulsions, may have respiratory failure

Extremely heavy or explosive

Sudden onset, high fever, deep coma, frequent convulsions Cerebral edema ​、 Cerebral hernia It causes death in 1-2 days, and this type accounts for about 5%.
In addition, a few patients showed Brainstem encephalitis ​、 meningitis And myelitis.

Etiology

Announce
edit
The pathogen of this disease belongs to the first subgroup of flavivirus in the family of peloviridae. It is spherical, with a diameter of 20~40nm, and is a single strand RNA virus. It has a lipid capsule membrane outside, and has hemagglutinin on the surface. It can agglutinate chicken red blood cells. The virus multiplies in the cytoplasm and is sensitive to temperature, ether, acid, etc. It can be passed on in the brain tissue of suckling mice, and can also grow in chicken embryos, monkey kidney cells, chicken embryo cells, and other cells. Its antigenicity is relatively stable.

Pathogenesis and pathophysiology

Announce
edit
Infected After the mosquito of JE virus bites the human body, the virus first proliferates in local tissue cells, lymph nodes and vascular endothelial cells, and constantly invades the blood stream, forming viremia. Whether it comes on or not depends on the number, virulence and immune function of the body of the virus. The vast majority of infected people do not get sick, showing recessive infection. When the amount of invading virus is large, the virulence is strong, and the immune function of the body is insufficient, the virus continues to multiply and spread throughout the body through the blood. Because the virus is neurotropic, it can break through the blood-brain barrier and invade the central nervous system, especially when the blood-brain barrier is low or there is a virus in the brain parenchyma.
The basic pathological changes are: (1) vascular endothelial cell damage, small blood vessels in the meninges and brain parenchyma can be seen to dilate, congest, bleed, and thrombosis, and the perivascular nested cell infiltration; (2) Nerve cells degenerated and necrosed, and after liquefaction and dissolution, they formed sieve shaped softening foci of different sizes; (3) Local glial cells proliferate to form glial nodules. Some patients' brains edema Serious, increased intracranial pressure or further cause Cerebral hernia [1]

clinical manifestation

Announce
edit
This disease has an incubation period of 4-21 days, generally 10-14 days. The typical course of JE is divided into four stages:

Incipient heat stage

The onset is acute, and the temperature rises sharply to 39~40 ℃, accompanied by headache , nausea and vomiting, some patients have lethargy or mental fatigue, and mild neck stiffness, the course of disease is 1-3 days.

Polar phase

The body temperature keeps rising, reaching more than 40 ℃. The initial symptoms gradually worsen, with obvious disturbance of consciousness, ranging from lethargy, lethargy to coma. The deeper the coma, the longer the duration, and the more serious the condition. Unconsciousness may first occur on the first to second days of the course of the disease, but most often occurs on the third to eighth days. Severe patients may have generalized convulsions, tetanic convulsions or tetanic convulsions paralysis A few can also be paralyzed. Severe patients may suffer from brain parenchyma inflammation (especially brain stem disease), hypoxia edema Cerebral hernia , hyponatremia encephalopathy, etc respiratory failure , manifested as irregular breathing rhythm, double inspiration, sigh like breathing, apnea, tidal breathing and mandibular breathing, and finally stopped breathing. Meningeal irritation sign can be found in physical examination. Pupils are slow to respond to light, disappear or dilate, abdominal wall and testis raising reflex disappear, deep reflex hyperfunction, pyramidal bundle sign such as Pap's sign can be positive.

convalescence

After the polar phase, the body temperature gradually dropped, and the mental and nervous system symptoms improved day by day. Severe patients still have mental retardation dementia , aphasia Dysphagia , tetanic spasm of limbs or Torsion convulsion A few patients may also have soft paralysis. After active treatment, most symptoms can be recovered within half a year.

Sequelae stage

About 5%~20% of patients have sequelae, which are found in severe patients such as high fever, coma and convulsion. The sequelae include aphasia paralysis And mental disorders were the most common.

Diagnosis and differential diagnosis

Announce
edit

Diagnostic basis

According to the epidemiological characteristics, epidemic season and children's susceptibility, high fever, coma, convulsion and respiratory failure And other clinical characteristics, combined with laboratory examination. The diagnosis depends on serological and pathogenic tests.
Blood routine examination: WBC disease increased moderately in the early stage, mostly (10-20) × 10 ∧ 9/L, neutrophils dominated, reaching 80%~90%, eosinophils decreased, which is different from common virus infection.
Cerebrospinal fluid examination: CSF routine examination and other virus susceptibility encephalitis Similarly, the pressure can be increased, the number of white blood cells is increased, (30~500) × 10 Λ 6/L, lymphocytes are the main type, and the severe patients are mainly multinucleated cells, often mixed with most red blood cells, the protein is normal or slightly increased, and the sugar and chloride are basically normal.
Imaging examination: On MRI, brain B often involves thalamus, brainstem, basal ganglia, hippocampus, cerebral cortex, cerebellum, subcortical white matter and spinal cord, of which thalamus, midbrain and basal ganglia are the most common lesions. Symmetrical involvement of thalamus is the characteristic manifestation of the focus of brain B. The lesions generally showed low signal on T1WI and high signal on T2WI. It is difficult to show the focus on T1WI or T2WI when the focus is early or the pathological change is slight. When there is bleeding, it usually shows spot or small piece of high signal. On DWI, the early manifestation is high signal, and the late focus is vascular edema Mainly, showing equal or low signal. On FLAIR, it usually shows high signal and maintains this signal feature for a long time. [2]
Serological examination: it is not easy to isolate JE virus in the blood, about 1/3 of the dead patients can be isolated from CSF, and almost no virus can be isolated from the survivors. Antibodies can be detected by hemagglutination inhibition test and neutralization test in the first week of onset, and complement binding antibody can be detected in the second week of onset yellow fever The cross reaction between viruses makes serodiagnosis difficult. At present, the detection of patient serum and CSF specific IgM antibodies with monoclonal antibodies can significantly increase the diagnostic sensitivity and specificity. [3]

differential diagnosis

enterovirus encephalitis : This kind of virus causes virus meningitis Besides, it is also viral encephalitis Is one of the common causes. It is commonly seen in summer and autumn, and is epidemic or sporadic. It is characterized by fever Consciousness obstacle , imbalance epilepsy Seizures and limbs paralysis Generally, it recovers quickly, and the symptoms will naturally relieve 2 to 3 weeks after the onset. Gastrointestinal symptoms at the early stage of the disease course, and viral nucleic acid detected by PCR in CSF can help diagnosis.
Herpes simplex Virality encephalitis : by Herpes simplex Virus infection. Acute onset, severe illness, fever, cough, etc upper respiratory tract infection The prodromal symptoms of Consciousness obstacle And early signs of focal nervous system damage. The typical imaging findings were located in the medial temporal lobe, frontal orbital surface, insular cortex and cingulate cortex. Detection of HSV specific antibodies in serum and cerebrospinal fluid is helpful for differentiation.
Toxic bacillary dysentery : The epidemic season of encephalitis B is the same as that of encephalitis B, mostly in summer and autumn, but the onset is more acute than that of encephalitis B, with high fever, convulsions shock Or coma, etc. Encephalitis B seldom occurs except for fulminant type shock 1%~2% saline enema can be used. If there is purulent or bloody stool, the diagnosis can be confirmed.
Purulent meningitis : The disease develops rapidly. Severe patients enter into coma within 1~2 days after onset. The meningeal irritation sign is obvious, and the skin often has petechiae. The cerebrospinal fluid is turbid with more than 90% neutrophils. Pathogenic bacteria can be found by smear and culture. The white blood cell count of peripheral blood picture was significantly increased, and the neutrophils were more than 90%. If it is meningococcal meningitis, it has seasonal characteristics. Early atypical cases are not easy to differentiate from encephalitis B, and they need to closely observe the condition and recheck cerebrospinal fluid.
Tuberculous meningitis : non seasonal, slow onset, long course, with tuberculosis History. Sugar and chloride in cerebrospinal fluid were reduced, and tuberculous bacillus could be found by film smear or culture. X-ray chest film, fundus examination and tuberculin test are helpful for diagnosis.

treatment

Announce
edit
At present, there is no specific etiological therapy, mainly supporting and symptomatic treatment.
Physical cooling should be actively taken for high fever, such as alcohol bath, head ice cap and ice salt water enema, to maintain the anal temperature at 38 ℃.
Optional anti convulsion epilepsy Medication, epilepsy In continuous state, adults can use intravenous injection of diazepam 20mg, children 0.2~0.3mg/Kg slowly, or add 80mg-100mg of diazepam into 5% glucose, and intravenous drip slowly. The dosage for adults in 24 hours shall not exceed 100mg. It can be maintained by chloral hydrate enema or intramuscular injection of phenobarbital sodium.
respiratory failure Continuous low flow oxygen inhalation and regular sputum aspiration should be carried out to keep the respiratory tract unobstructed. Early tracheotomy should be carried out for excessive secretion of the respiratory tract. Centrality respiratory failure Lobeline, nikethamide or ritalin can be used alone or in combination. Antibiotics can be used to treat coma with lung infection, and ventilator can be used to assist breathing in severe patients.
Cerebral edema Dehydration and intracranial pressure reduction treatment should be given, with 20% mannitol 125-250ml, once every 6-8 hours, and rapid intravenous drip; Furosemide is 20-40mg, once every 6-8 hours, or mannitol and furosemide are used alternately. Corticosteroids can be used for short term in severe patients.
Intramuscular injection of α - interferon 500000~5 million U, or 50000 U/Kg, 3~5 days as a course of treatment. It can shorten the course of disease and reduce the mortality. It has also been reported that intrathecal injection of interferon is effective, but the efficacy remains to be confirmed.

prognosis

Announce
edit
Patients with Parkinson's syndrome and early respiratory failure have a poor prognosis. Severe patients generally die 7 to 10 days after the disease.

prevention

Announce
edit
Planned immunization for children is safe and effective. It is feasible to vaccinate people who work or travel in high-risk areas at least three times a month in advance during the epidemic period. The application of insecticides to reduce mosquito density and vaccination of pigs are also ways to reduce the disease. It is necessary to isolate the sick.

nursing

Announce
edit

General care

Strict bed rest, different diet according to different disease stages, light diet at the initial stage and extreme stage, coma and Dysphagia Patients should be given nasal feeding or intravenous infusion, and nutrition should be gradually increased during the recovery period, with a high calorie diet.

Disease observation

Observe the state of consciousness convulsions Episode aura, attack frequency and duration, observation Intracranial hypertension and Cerebral hernia The focus should be on the pupil size, whether the two sides are symmetrical, and the response to light. Accurately record the inflow and outflow, and observe whether there are complications.

Symptomatic nursing

Body temperature: the body temperature of patients with encephalitis B is not easy to drop, and comprehensive measures are often taken to control body temperature, including physical cooling and drug cooling.
Convulsion: It should be detected early and treated in time. If convulsions are caused by respiratory tract secretion obstruction, sputum aspiration and oxygen inhalation should be given; convulsions Or in case of convulsions, pay attention to prevent suffocation and trauma.
Respiratory failure: For patients with respiratory failure, keep the respiratory tract unobstructed and take oxygen in time. If the above treatment fails, tracheal intubation, tracheotomy or artificial respirator should be used for treatment.

Nursing of recovery period and sequelae

For patients in the recovery period, attention should be paid to increasing nutrition, preventing secondary infection, observing the patients' mental state, and the recovery of various physiological and motor functions. Those who have left mental and neurological sequelae can be treated with combination of Chinese and Western medicine. The patients should be encouraged, cared for and guided to perform functional exercises to help them recover as soon as possible. [4]