cerebrospinal infiltration
Introduction
Introduction Epidemic cerebrospinal meningitis is referred to as epidemic cerebrospinal meningitis. It is a purulent meningitis caused by meningococcus. Clinical manifestations include fever, headache, vomiting, skin and mucous membrane defects, ecchymosis and neck stiffness. The disease was described in 1805 by Vieusseaux, Switzerland. In 1887 Weichselbaum isolated meningococcus from the cerebrospinal fluid. In 1896, Li Tao officially reported in Wuchang.
Cause
Cause
(I) Pathogenesis The development of meningococcal bacteria from the nasopharynx depends on the interaction between human pathogens. If the human body is healthy and the immunity is normal, the bacteria can be quickly eliminated or become a carrier. If the body lacks specific bactericidal antibodies, or the virulence of the bacteria is strong, the bacteria invade the bloodstream from the nasopharynx to form bacteremia or sepsis. Re-invasion of the cerebrospinal membrane to form suppurative meningitis.
At present, it is considered that the deficiency or reduction of congenital or acquired IgM, the lack of complement C3 or C3C9 is easy to cause onset, even recurrent or violent, and some people think that the increase of specific IgA and its immune complex with pathogens is also Causes of morbidity.
In the past, the type of septicemia called Waterhuose-Friderichsen syndrome was caused by acute adrenal insufficiency caused by adrenal hemorrhage and necrosis. Recent studies have suggested that mainly due to the rapid proliferation of meningococcus in the capillary endothelial cells to release endotoxin, resulting in microcirculatory disorders, and activation of the coagulation system leads to DIC. At the same time, endotoxin also activates the humoral and cell-mediated reaction system, and a systemic Schwarzmans reaction occurs. Adrenal cortical hemorrhage is the result of a systemic Schwarzman reaction. Microcirculatory disorders, such as those occurring in the systemic and visceral systems, are clinically characterized by outbreaks of sepsis; for example, meningeal lesions are predominantly formed by cerebrovascular injury; or so-called mixed type.
Chronic sepsis type and its causes of chronic and recurrent episodes, in addition to the lack of bactericidal antibody formation after acute infection, its complement system C6, C7 defects may also be an important cause.
(B) pathological changes in the sepsis, the main lesions are vascular endothelium damage, vascular wall inflammation, necrosis and thrombosis simultaneously with perivascular hemorrhage; skin, subcutaneous tissue, mucosa and serosal and other focal bleeding.
In the autopsy of deaths of septicemia, a large number of Gram-negative diplococcus were found in the vascular endothelial cells and in the lumen of the skin. The skin and visceral vascular damage were severe and extensive, and the endothelial cells were shed and necrotic. There was fibrin-white blood cell-platelet formation in the vascular lumen. The thrombus. Extensive bleeding in the skin, lungs, heart, gastrointestinal tract and adrenal glands. Myocarditis and pulmonary edema are also common.
The lesions in the meningitis are mainly pia mater. Early hyperemia, a small amount of serous exudation and focal small bleeding points. In the later stage, there are a large amount of fibrin, neutrophils and plasma extravasation. The lesions are mainly on the surface of the brain and the base of the skull. Due to the viscous and purulent lesions of the skull base, it can cause meningeal adhesions, causing increased attention to nerves, abductor nerves and oculomotor nerves, facial nerves, auditory nerves and other cranial nerve damage. Degenerative lesions occur in the surface of brain nerve tissue due to damage to endotoxin. In addition, inflammation can also invade brain tissue along the vessel wall, causing congestion, edema, focal neutrophil infiltration, and hemorrhage. In cases of fulminant meningitis, the lesions are mainly brain tissue, with obvious congestion and edema, and increased intracranial pressure. When the edema brain tissue protrudes into the intracranial hole, a large occipital hole or a canopy hole is formed.
A small number of children due to ventriculitis, occlusion of the brain aqueduct, causing cerebrospinal fluid circulation blocked and hydrocephalus.
In addition to the cerebrospinal membrane, other organs may also have migratory suppurative lesions, including endocarditis, pericarditis, septic arthritis, pneumonia, eyeball and so on.
Examine
an examination
Related inspection
Spinal MRI examination of the spine
The incubation period is 1 to 7 days, usually 2 to 3 days. The condition is complex and variable, varying in severity, and can generally be manifested in three clinical types, namely common type, fulminant type, and chronic sepsis type.
(1) The ordinary type accounts for about 90%. The course of the disease can be divided into upper respiratory tract infection period, sepsis period and meningitis period, but it is difficult to divide due to acute onset, rapid progress and clinical practice.
1. Upper respiratory tract infection: Most patients do not develop any symptoms. Some patients have sore throat, congestion of the nasopharyngeal mucosa and increased secretions. Nasopharyngeal swab culture can often find pathogens, but it is difficult to diagnose.
2. Septicemia: Patients often have no prodromal symptoms, chills, high fever, headache, vomiting, and general malaise. Toxic symptoms such as muscle soreness, loss of appetite and apathy. Young children are crying, noisy, restless, skin allergies and convulsions. A small number of patients have joint pain or arthritis, and splenomegaly is common. About 70% of patients have visible spots or ecchymoses on the skin and mucous membranes. In severe cases, ecchymosis and ecchymoses can rapidly expand, and large pieces of necrosis occur due to thrombosis. About 10% of patients often develop herpes simplex in the labial and other areas on the first few days of the disease.
3. Meningitis: Most patients with sepsis have meningeal irritation around 24 hours. This period is persistently high fever, severe headache, frequent vomiting, skin allergies, fear of light, arrogance and convulsions, and coma. Blood pressure can be increased and the pulse slowed down. Inflammatory stimulation of the meninges, manifested as posterior neck pain, neck stiffness, angular arch reversal, Klinefelter and Brine's sign positive.
Infants have many episodes. In addition to high fever, refusal of milk, irritability and cries, convulsions, diarrhea and cough are more common in adults, and meningeal irritation may be absent. The front bronchi is prominent and helps to diagnose. However, sometimes due to frequent vomiting and loss of water, only the anterior bronchi sag, which makes diagnosis difficult.
(B) fulminant: a small number of patients with acute onset, if the condition is dangerous, if not rescued in time, often within 24 hours or even within 6 hours of life-threatening, this type of mortality rate of 50%, infants and young children up to 80%.
1. fulminant sepsis (shock type): this type is more common in children. The protrusions are hot, headache, vomiting, and the spirit is extremely wilting. Often in the short term, a wide range of sputum, ecchymosis, and rapid fusion into large pieces, subcutaneous bleeding, or followed by large pieces of necrosis. The complexion is gray, the lips and the fingertips are purple, the limbs are cold, the skin is patterned, the pulse is fine, the blood pressure drops, and even the blood is not measured. There is a lack of meningeal irritation. Most of the cerebrospinal fluid is clear, the number of cells is normal or slightly increased, and blood culture is often positive.
2. fulminant meningoencephalitis: also seen in children. In addition to severe symptoms of poisoning, patients frequently convulsed quickly into a coma. There are positive pyramidal tract signs and bilateral reflections. Blood pressure continues to rise and some patients develop cerebral palsy. When the occipital foramen is sacral, the cerebellar tonsils are inserted into the large hole of the occipital bone, and the medulla is compressed. At this time, the patient's coma is deepened, the pupil is obviously reduced or enlarged, or the pupil is not neat, the photoreaction is slow. The bilateral muscle tension is increased or stiff, the upper limbs are more internal rotation, and the lower limbs are stretched and straight. Irregular breathing, or unevenness, or pause, become soaking, or nodding, or tidal breathing. Such breathing often indicates a sudden stop of breathing. In addition to the above-mentioned increased intracranial pressure, the same side of the pupil is enlarged by the pressure of the oculomotor nerve, the photoreaction disappears, the eyeball is fixed or abducted, and the contralateral limb is paralyzed. Then there is respiratory failure.
3. Mixed type: It is the most serious type of this disease, the mortality rate is often as high as 80%, and there are two kinds of clinical manifestations of fulminant, often appearing simultaneously or sequentially.
(C) chronic sepsis is rare in this type. It occurs mostly in adults, and the course of disease is delayed for weeks or months. Repeated chills, high fever, skin blemishes, and ecchymoses. Joint pain is also common, and joint pain is exacerbated during fever. Meningitis, whole heart disease or nephritis can also occur.
Diagnosis
Differential diagnosis
(1) Other purulent meningitis: pneumococcal meningitis, influenza bacilli meningitis, staphylococcal meningitis and many other infections exist in the body. For example, pneumococcal meningitis mostly occurs on the basis of pneumonia and otitis media; staphylococcal meningitis mostly occurs in the course of staphylococcal septicemia. The exact diagnosis depends on cerebrospinal fluid, blood bacteriology and immunological examination.
(B) virtual meningitis: some patients with acute infection may have meningeal irritation when there is severe toxemia, but except for the slightly higher pressure of cerebrospinal fluid, the rest are normal.
(3) Tuberculous meningitis: a history of tuberculosis. Slow onset, accompanied by symptoms such as low fever, night sweats, weight loss, no wandering and herpes. The number of cells in the cerebrospinal fluid is tens to hundreds of cells, mainly lymphocytes. When the cerebrospinal fluid is placed in a test tube for 12 to 24, a film is formed, and the anti-acid staining of the film and the cerebrospinal fluid precipitation smear can detect the Mycobacterium tuberculosis.
(4) Epidemic encephalitis B: The incidence is mostly from July to September. There is a history of mosquito bites. After the onset, the brain parenchymal damage is serious. The convulsions and coma are more common, and the skin is generally innocent. The cerebrospinal fluid is clear in the early stage and the late micro-sputum. The number of cells is 0.1-0.5×109/L, rarely exceeds 1×109/L, the protein is slightly increased, the sugar is normal or slightly higher, and the oxide is normal. Diagnosis depends on double serum complement fixation test, hemagglutination inhibition test, etc. and brain tissue isolation virus.
