viral hemorrhagic fever
Introduction
Introduction to viral hemorrhagic fever Viral hemorrhagic fever is a natural epidemic disease caused by a group of arboviruses. It is characterized by fever, hemorrhage and shock. These diseases are widely distributed in the world, clinical manifestations are more serious, and the mortality rate is very high. At present, more than ten kinds have been found in the world. Their pathogens, parasitic hosts and routes of transmission vary, and there are some differences in clinical manifestations, which are often prevalent in certain areas. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of transmission: insect vector transmission Complications: blood in the stool, shock, meningitis
Cause
Viral haemorrhagic fever
(1) Causes of the disease
Viral hemorrhagic fever is a natural epidemic disease caused by a group of arboviruses, with fever, hemorrhage and shock as the main clinical features.
(two) pathogenesis
At present, it is believed that the direct damage of the virus is the main one. After the virus enters the human body, it will produce viremia through replication and proliferation, causing damage to the whole body capillary endothelial cells, increasing vascular permeability and fragility, causing bleeding, edema and shock. The clinical manifestations of the series, viremia can also cause degeneration and necrosis of parenchymal cells in various organs, and lead to dysfunction, the main pathological changes are telangiectasia, congestion, hemorrhage, intraluminal fibrin or Platelet thrombosis, degeneration and necrosis of parenchymal cells: necrosis of the center of the hepatic lobe, focal or point necrosis, telangiectasia and hyperemia of the alveolar wall, protein exudate in the alveoli, fibrin thrombosis in the pulmonary capillaries The size of the kidney is enlarged. The glomerular vessel wall and the renal sac basal thickening can be seen by microscopic examination. In addition to the autolysis phenomenon, the proximal renal tubular epithelial cells can be seen with turbidity and a small amount of red blood cells in the tube, and renal medulla interstitial edema. The blood vessels dilate, thus squeezing the surrounding renal tubules, narrowing or even occluding the lumen, and having segmental degeneration of the renal tubular epithelium Death, in addition, myocardium, adrenal gland, pancreas, etc. have varying degrees of degeneration, necrosis, inflammatory cell infiltration in the necrotic area is not obvious, meninges are non-suppurative meningitis changes, brain parenchyma edema, telangiectasia congestion, peripheral bleeding and lymph Cell infiltration, cortical and brain stem have varying degrees of neuronal degeneration, neuroblastic phenomena and microglia proliferation.
Prevention
Viral hemorrhagic fever prevention
Prevention of viral hemorrhagic fever should take comprehensive measures, regularly kill the rats, regularly kill the animals in vitro, reduce the density of cockroaches, enter the desert, and the farmer or forest area workers should do personal protection, prevent bites, contact with sick animals or The patient's blood should be worn with gloves and no raw milk. Vaccination is the main measure to prevent this disease. The domestically inactivated milk rat brain can be used to refine the vaccine. In the population, the positive rate of antibody after three injections can be tested. More than 70%.
Complication
Viral hemorrhagic fever complications Complications, hemorrhagic shock, meningitis
1. Cavity bleeding hematemesis, blood in the stool is the most common, can cause secondary shock, abdominal bleeding, nasal and vaginal bleeding are more common.
2. Central nervous system complications include encephalitis and meningitis caused by viral invasion of the central nervous system, cerebral edema caused by shock, clotting dysfunction, electrolyte imbalance and high blood volume syndrome in shock and oliguria. Hypertensive encephalopathy and intracranial hemorrhage can cause headache, vomiting, disturbance of consciousness, convulsions, respiratory rhythm changes or hemiplegia. CT examination is helpful for the above diagnosis.
3. Pulmonary edema This is a very common complication, and there are two clinical situations.
(1) Acute Respiratory Distress Syndrome (ARDS): This is a pulmonary capillary injury. Increased permeability leads to massive exudation of the pulmonary interstitial. In addition, thrombosis of microvessels in the lungs and reduction of alveolar surfactant production can contribute to ARDS. The clinical manifestations are shortness of breath, 30 to 40 beats/min. There is no obvious cyanosis and pulmonary voice in the early stage. The hair can be found in the middle stage. The lungs can smell bronchial breath sounds and dry and wet voices. X-ray films can be seen. Side spotted or flaky shadow, the lung field is shaded thick, and the edge is thin, glassy, blood gas analysis arterial oxygen partial pressure (PaO2) is reduced to below 8.0kPa (60mmHg), and progressive reduction, alveolar arterial pressure is obvious Increased, up to 4.0kPa (30mmHg) or more, common in shock and oliguria, recent reports of Hantavirus lung syndrome in New Mexico and other places, with ARDS as the main performance, often within 2 to 6 days of onset Death due to respiratory distress leading to acute respiratory failure.
(2) heart failure pulmonary edema: can be caused by damage to the pulmonary capillaries, a large amount of exudate in the alveoli, can also be caused by high volume or myocardial damage, mainly manifested by increased breathing, cough foam-like pink sputum, cyanosis And full lungs.
4. Hemorrhagic fever caused by pleural effusion and atelectasis is common. Kanerva examined 125 patients with PUUV-induced HFRS and found that 28% of patients had pleural effusion or atelectasis, while pulmonary edema was rare. These patients have more obvious hypoproteinemia, so it is believed that capillary leakage and inflammation may be the cause of abnormal lungs.
5. Secondary infections are more common in oliguria and early polyuria. Pulmonary and urinary tract infections and sepsis are more common. They are caused by decreased immune function and catheterization, which may cause secondary shock and worsen the condition.
6. Spontaneous renal rupture occurs mostly in the oliguria period, due to severe renal medullary hemorrhage, often due to nausea, vomiting or cough, etc., causing a sudden increase in abdominal or thoracic pressure, causing an increase in renal blood pressure and promoting bleeding Suddenly sitting up or turning over, causing the psoas muscle to contract sharply, the kidney is squeezed and easily cause kidney rupture. The clinical manifestation is that the patient feels pain in the waist or abdomen, the local area is obviously swollen, the abdomen can touch the mass, and the lumbar muscles are tense. Restricted activity, severe bleeding, blood pressure drops, cold sweat dripping, if the blood infiltrates into the abdominal cavity, there may be signs of peritoneal irritation, abdominal wear with blood, B-ultrasound can be found in the renal and abdominal cavity mass in the flat section, if timely surgery Can reduce the mortality rate.
7. Heart damage and heart failure Hantavirus can invade the myocardium and cause myocardial damage. Clinically, it is often bradycardia and arrhythmia. Because of high blood volume syndrome, pulmonary edema, etc., the myocardial burden is too heavy, so heart failure can occur. .
8. Liver damage 4% ~ 60% of patients with elevated ALT, a small number of patients with jaundice or significant liver damage, liver damage is more common with SEOV infection, is caused by viral damage to the liver.
9. Hyperosmotic non-ketotic coma Very few patients with HFRS appear indifferent or oligomic during periods of oliguria or polyuria, sluggish, lethargy or even coma, check blood glucose is significantly increased, often >22.9 ~ 33.6mmol / L, blood sodium > 145mmol / L, urine ketone negative, plasma osmotic pressure > 350mmol / L, this is the HFRS patients pancreatic cells infected by the virus to reduce insulin secretion, or excessive use of glucocorticoids, intravenous sugar, excessive sodium and excessive diuretic lead to dehydration Caused.
Symptom
Viral hemorrhagic fever symptoms Common symptoms Cheeks and upper chest congestion, intestinal bleeding, nosebleeds, hypotension, proteinuria, papules, bloody bleeding, fever, and bleeding
Various viral hemorrhagic fever, although there are differences in clinical manifestations, but have the following basic performance.
1. Fever This is the most basic symptom of this group of diseases. Different hemorrhagic fever, fever duration and heat type are not exactly the same. Mosquito-mediated hemorrhagic fever is mostly bimodal fever, and various symptoms follow the second fever. Intensified, epidemic hemorrhagic fever and Xinjiang hemorrhagic fever are mostly persistent fever.
2. Bleeding and rash all kinds of hemorrhagic fever have bleeding, rash phenomenon, but the location of bleeding, rash, time and extent are different, lighter only a few bleeding points and rash, severe cases can occur gastrointestinal tract , major bleeding in the respiratory tract or genitourinary system, the bleeding and rashes of hemorrhagic fever diseases seen in China and other regions are briefly described as follows:
(1) epidemic hemorrhagic fever: in the fever period of 1 to 5 days after onset, it is acute disease, facial, buccal and upper chest congestion, flushing, conjunctival hyperemia, such as drunkenness, fine bleeding spots in the skin mucosa, often distributed In the upper jaw, conjunctiva, underarm and sputum, clustered or strip-like arrangement, some patients with ecchymosis at the puncture and compression site, more pharyngeal congestion, significant conjunctival edema, more than 95% of patients with beam arm The test is positive, and the symptoms are aggravated during the hypotension period of 5 to 8 days after the onset of the disease. At this time, the congestion phenomenon subsides, and the bleeding phenomenon is aggravated, and the skin mucosal bleeding point is increased, which can be merged into ecchymosis, and may be accompanied by gastrointestinal bleeding, lung. Bleeding, etc., into the oliguria period (more on the 8th to 12th day after the disease), the bleeding phenomenon is more significant, the skin of the oppressed area can be seen with large ecchymosis, and can cause massive bleeding, such as hemoptysis, hematemesis, blood in the stool, nosebleeds Wait.
(2) Dengue hemorrhagic fever: Dengue virus can cause dengue fever without bleeding tendency, but in the past 20 years, dengue fever in Southeast Asia is often accompanied by severe epidemics of severe bleeding and shock, called "dengue hemorrhagic fever" Dengue hemorrhagic fever is a clinical syndrome. The main symptoms are high fever, hepatosplenomegaly, shock and hemorrhage. Most patients have scattered tendons in the limbs, face, armpits and soft palate, sometimes fused into sputum. Spot, in addition, erythema, maculopapular rash and wheal-like rash can occur, some patients may have nosebleeds, bleeding gums, gastrointestinal bleeding and hematuria.
(3) Xinjiang hemorrhagic fever: the patient is accompanied by facial and upper chest skin congestion, flushing, chest, back, armpit, face, neck and limbs with sputum and ecchymosis, more than a line under the armpit Arranged, the bleeding point is more on the upper body, less in the lower body, eyes, soft palate and gums are also defective, hematoma and ecchymosis can be seen at the injection site, and the conjunctiva of the eyeball is edematous.
(4) Far eastern hemorrhagic fever: The disease is caused by arboviruses. The vector is rodent, mainly in the Americas and North Korea. Sudden onset, fever, headache, low back pain and other systemic symptoms. Defects appear in the conjunctiva and skin (especially the ankle).
(5) Argentinian hemorrhagic fever: The disease is caused by the Junin virus of the arbovirus. The vector is sputum, fever, headache, low back pain, gums and nosebleeds.
(6) Belivian hemorrhagic fever: This disease is caused by the Machup virus of arbovirus. The vector is rodent. It has fever, headache, joint pain and muscle pain. Some patients feel skin allergies. Even after exposure to light, it can cause pain in the skin, there is obvious conjunctivitis, edema around the eyelids, but there is no defect in the skin mucosa, there may be gastrointestinal bleeding, and diffuse alopecia may occur during the recovery period.
3. Hypotension shock can occur in various hemorrhagic fevers, but the frequency and extent of occurrence are very different. Epidemic hemorrhagic shock occurs most and severely.
4. Renal failure is the most serious kidney damage caused by epidemic hemorrhagic fever. Other hemorrhagic fever can also have different degrees of renal damage, but it is mild, only mild to moderate proteinuria.
Examine
Examination of viral hemorrhagic fever
1. Leukocytes and thrombocytopenia, immature cells can appear in the surrounding blood.
2. Some patients have a slightly longer clotting time.
3. Early stage patients can have different degrees of proteinuria, individual tube type, blood urea nitrogen and creatinine increased.
4. Mild liver dysfunction can occur in the early stage of the disease, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are elevated, and serum bilirubin is elevated in some patients.
5. Specific antigen antibody detection using ELISA double antibody sandwich method, reverse hemagglutination test can detect circulating antigen in serum, can also detect specific IgM antibody by antibody capture ELISA for early diagnosis, for suspicious results or patients in newly infected areas A complement fixation test or a neutralization test is needed to confirm the diagnosis.
Diagnosis
Diagnosis and identification of viral hemorrhagic fever
Clinical diagnosis can be comprehensively analyzed based on epidemiological data, clinical manifestations, and laboratory findings, and serological or virological evidence must be available for diagnosis.
The febrile period should be differentiated from upper respiratory tract infection, sepsis, acute gastroenteritis and dysentery. The shock phase should be differentiated from other septic shocks. The oliguria phase is differentiated from acute nephritis and other causes of acute renal failure. Patients with peptic ulcer bleeding, thrombocytopenic purpura and other causes of DIC identification, ARDS as the main manifestation should pay attention to other causes caused by differences, abdominal pain as the main signs should be identified with surgical acute abdomen.
