Epidemic Hemorrhagic Fever

　　Yiqian fever is caused by the invasion of warm and toxic evil into the blood vessels, damaging the heart and kidneys. It can occur throughout the year, but it is more common in winter and spring. Young and middle-aged males are more common. There is a history of contact with rodents or outdoor work. The onset is abrupt, with high fever and aversion to cold.

　　Hemorrhage in cavities Hemorrhage, hematochezia, and hematochezia are the most common, which can cause secondary shock. Abdominal hemorrhage, nasal and vaginal hemorrhage, and other hemorrhages are relatively common.

　　Complications of central nervous system include encephalitis and meningitis caused by viral invasion of the central nervous system in the early stage of the disease, cerebral edema, hypertensive encephalopathy, intracranial hemorrhage, and other complications caused by shock, coagulation dysfunction, electrolyte disturbance, and high-volume syndrome during the shock phase and oliguria phase. Headache, vomiting, disturbance of consciousness, convulsions, changes in respiratory rhythm, or hemiplegia may occur. CT examination is helpful for the above diagnosis.

　　Pulmonary edema is a common complication of the disease, and there are two types in clinical practice.

　　Acute respiratory distress syndrome (ARDS): This is caused by pulmonary capillary injury, increased permeability leading to large amounts of exudation in the pulmonary interstitium. In addition, the formation of thrombi in the small blood vessels in the lungs and the reduction in the production of surfactant on the alveolar surface can also lead to ARDS. Clinical manifestations include tachypnea, 30-40 times/min. In the early stage, there is no significant cyanosis and lung sounds. In the middle stage, cyanosis may appear, and bronchial breathing sounds and moist and dry? sounds can be heard throughout the lungs. Chest X-ray shows bilateral punctate or patchy shadows, with dense shadows in the outer part of the lungs and thin edges, resembling ground glass. Arterial oxygen partial pressure (PaO2) decreases to below 8.0 kPa (60 mmHg) and continues to decrease. Alveolar-arterial pressure increases significantly, reaching above 4.0 kPa (30 mmHg). It is common during the shock phase and oliguria phase. A recent report from the United States describes hantavirus pulmonary syndrome occurring in New Mexico and other places, with ARDS as the main manifestation. Death often occurs between the 2nd and 6th days of illness due to acute respiratory failure caused by respiratory distress.

　　Heart failure: It can be caused by damage to the pulmonary capillaries, large amounts of exudation in the alveoli, or high volume or myocardial damage. The main manifestations are increased respiratory rate, coughing up frothy pink sputum, cyanosis, and full lung? sounds.

　　Pleural effusion and atelectasis Hemorrhagic fever caused by Puumala virus is common. Kanerva examined 125 patients with HFRS caused by PUUV and found that 28% of patients had pleural effusion or atelectasis, and pulmonary edema was rare. These patients all have relatively obvious hypoproteinemia, and capillary leakage and inflammation are considered to be the causes of pulmonary abnormalities.

　　Secondary infection It is more common during the oliguria phase and early polyuria phase, and is more common in pulmonary and urinary tract infections, as well as sepsis. This is due to decreased immune function and urinary catheterization and other procedures, which are prone to secondary shock and exacerbation of the condition.

　　Spontaneous renal rupture It commonly occurs during the oliguria phase due to severe renal medullary hemorrhage. It often occurs due to sudden increases in abdominal or thoracic pressure caused by nausea, vomiting, or coughing, which increases intravascular pressure in the kidneys and promotes hemorrhage. Sudden sitting up or turning over can cause the psoas muscle to contract sharply, and the kidneys are easily damaged, leading to renal rupture. Clinical manifestations include sudden severe pain in the lower back or abdomen, and in severe cases, blood pressure drops and profuse sweating. If blood leaks into the abdominal cavity, peritoneal irritation signs may appear, and percutaneous aspiration shows fresh blood. Ultrasound examination can detect liquid flat segments in the renal perihepatic and abdominal masses. If surgery is performed in time, the mortality rate can be reduced.

　　Cardiac damage and heart failure The Hantavirus can invade the myocardium and cause myocardial damage, which is commonly manifested as bradycardia and arrhythmia in clinical practice. Due to overburden on the myocardium caused by hyper volume syndrome, pulmonary edema, and other factors, heart failure may occur.

　　Liver damage ALT levels are elevated in 4%-60% of patients, and a few patients may experience jaundice or significant liver function impairment. Liver damage is most common in SEOV infection, which is caused by viral damage to the liver.

　　Hyperosmolar nonketotic coma A small number of HFRS patients may appear apathy, drowsiness, and even coma during the oliguria or polyuria phase. Blood glucose levels are significantly elevated, often greater than 22.9-33.6 mmol/L, blood sodium >145 mmol/L, urine ketones negative, and plasma osmotic pressure >350 mmol/L. This is due to the invasion of viral particles into the pancreatic β cells, leading to decreased insulin secretion, or excessive use of corticosteroids, intravenous glucose and sodium supplementation, excessive diuresis, and dehydration.

　　Epidemic hemorrhagic fever can occur throughout the year, but it is more prone to epidemic in winter and spring. Young and middle-aged males are more common. There is a history of contact with rodents or outdoor work.

　　The onset is abrupt, with high fever and aversion to cold, characterized by 'five pains' (headache, orbital pain, lumbar pain, abdominal pain, and muscle and joint pain), 'five reds' (red eyes, red throat, red face, red cheeks, and red upper chest), as well as thirst, vomiting, and rash on the skin and mucous membranes.

　　Typical cases have five stages, namely, fever stage, hypotensive shock stage, oliguria stage, polyuria stage, and recovery stage. However, the severity and duration of each stage may vary, and some stages may overlap or not appear.

　　Laboratory examination: peripheral blood count shows an increase in total white blood cells and abnormal lymphocytes; urine examination shows protein, red blood cells, white blood cells, and casts; immunological examination shows early positivity of IgM antibody or a fourfold increase in IgG antibody titer; positive detection of specific antigens in blood and urine sediment.

　　Prevention of epidemic hemorrhagic fever

　　(One) Eradicate and Prevent Rodents: Eradication of rodents is the key to preventing the spread of the disease. In epidemic areas, it is necessary to organize the masses to carry out rodent eradication at the same time within the specified time. The timing of rodent eradication should be before the peak period of the disease (May to June and October to December). In spring, emphasis should be placed on eradicating domestic rodents, and in early winter, emphasis should be placed on eradicating wild rodents.

　　Currently, the commonly used methods include mechanical methods and poison bait methods. Mechanical methods can use rat traps and rat cages to kill rodents. The poison bait method mainly uses food that rodents like as bait, mixed with rodenticide at a certain ratio to make poison bait, and placed in rat holes or places where rodents frequently appear. Common rodenticides for domestic rodents include sodium diphacinone, brodifacoum, and for wild rodents include zinc phosphide, chlorophacinone, etc. The poison bait method is effective in eradicating rodents, but the disadvantage is that improper use can cause poisoning in humans and animals. Therefore, someone should be on guard for the first three days after placing poison bait in the field, and any excess poison bait should be collected and destroyed after three days. In the home, place poison bait before going to bed at night and remove it during the day, as rodents have a very strong reproductive capacity, so rodent control should be persistent, and any relaxation may result in all previous efforts being wasted.

　　Under the premise of rodent control, do a good job of rodent prevention at the same time. The bed should not be against the wall, sleep on high beds, dig rodent-proof ditches outside the house to prevent rodents from entering the house and courtyard. When building or renovating houses, rodent-proof facilities should be installed.

　　(Two) Eradicate and Prevent Ticks: Keep the house clean, well-ventilated, and dry, and regularly spray organic phosphorus insecticides like DDD to eradicate ticks and clear away grass piles indoors and outdoors.

　　(Three) Strengthen Food Hygiene: Do a good job of food hygiene, sterilization of utensils, and food preservation. Prevent rodent excrement from contaminating food and utensils, and leftover food must be heated or steamed before it can be eaten.

　　(Four) Do a Good Job of Disinfection: The blood, urine, and carcasses of the host animals, as well as their excrement, of fever patients should all be disinfected to prevent environmental contamination.

　　(Five) Pay Attention to Personal Protection: Do not touch rodents and their excrement with bare hands in the epidemic area, do not sit or lie on grass piles, prevent skin injury during work, and disinfect and bandage the wound after injury. When working outdoors, wear socks, tighten the legs and cuffs, to prevent tick bites.

　　Items of Examination Needed for Epidemic Hemorrhagic Fever

　　Urine Routine, Urine Sediment, Urea, Urea Nitrogen, Alanine, Electrocardiogram, Intraocular Pressure, Thrombin Time, Clotting Time, Fibrinogen

　　Laboratory Examination

　　1. Blood Routine

　　(1) White Blood Cell Count: The count is mostly normal in the first 1 to 2 days of the disease, and gradually increases after the 3rd day of the disease, reaching (15～30)×10^9/L, with a few severe patients reaching (50～100)×10^9/L.

　　(2) White Blood Cell Classification: In the early stage of the disease, there is an increase in neutrophils and nuclear left shift, with toxic granules. Severe patients may show immature cells in a leukemic reaction. On the 4th to 5th day of the disease, there is an increase in lymphocytes, and a large number of atypical lymphocytes appear. Since atypical lymphocytes can also appear in other viral diseases, they cannot be used as the main basis for disease diagnosis.

　　(3) Hemoglobin and Red Blood Cells: Due to plasma exudation, blood becomes concentrated, so from the late stage of fever to the hypotensive shock period, the levels of hemoglobin and red blood cells increase, reaching above 150g/L and 5.0×10^12/L.

　　(4) Platelets begin to decrease from the second day of the disease, generally at around (50～80)×10^9/L, and atypical platelets can be seen.

　　2. Urinalysis

　　(1) Urinary Protein: It can appear as early as the second day of the disease. Urinary protein is often detected between the fourth and sixth day of the disease, with a sudden appearance of a large amount of urinary protein, which is very helpful for diagnosis. In some cases, a membrane-like substance appears in the urine, which is a precipitate mixed with a large amount of urinary protein, red blood cells, and shed epithelial cells.

　　(2) Microscopic Examination: Red blood cells, white blood cells, and casts can be seen. In addition, giant fused cells can be found in the urine sediment, which are caused by the fusion of urinary tract shed cells induced by the envelope glycoprotein of the EHF virus under acidic conditions. EHF virus antigens can be detected in these fused cells.

　　3. Blood Biochemical Examination

　　(1) Blood Urea Nitrogen and Creatinine: Most patients start to show an increase in blood urea nitrogen and creatinine during the hypotensive shock phase, while a few patients may show an increase in the late febrile phase. They reach their peak at the end of the transition period and begin to decrease during the late polyuria phase.

　　(2) Blood Acid-Base Balance: During the febrile period, respiratory alkalosis is common in blood gas analysis, which is related to fever and overventilation. During the shock and oliguria phases, metabolic acidosis is predominant.

　　(3) Electrolytes: Blood sodium, chloride, and calcium are mostly reduced in all stages of the disease, while phosphorus, magnesium, and others increase. Blood potassium remains at a low level during the febrile and shock phases, increases during oliguria, and then decreases again during polyuria. However, a few patients may still have low blood potassium levels during oliguria.

　　(4) Coagulation Function: During the onset of fever, there is a decrease in platelets, with reduced adhesion, aggregation, and release functions. If DIC occurs, platelets often decrease to below 50×10^9/L. During the hypercoagulable phase of DIC, the coagulation time shortens, while during the consumptive hypocoagulable phase, fibrinogen decreases, prothrombin time and thrombin time prolong, and during the hyperfibrinolysis phase, the level of fibrin degradation products (FDP) increases.

　　4. Special Examinations

　　(1) Virus Isolation: During the febrile period, serum, blood cells, and urine samples can be inoculated into Vero-E6 cells or A549 cells to isolate Hantavirus.

　　(2) Antigen Testing: In the early stage of the disease, the serum, peripheral blood neutrophils, lymphocytes, and monocytes, as well as urine and urine sediment cells, can be used with the polyclonal or monoclonal antibodies of the Hantavirus to detect Hantavirus antigens. Common methods include immunofluorescence or ELISA, while colloidal gold methods are more sensitive.

　　(3) Specific Antibody Detection: Includes the detection of specific IgM or IgG antibodies in serum, with IgM antibody at a dilution of 1:20 considered positive, detectable as early as the second day of onset. IgG at a dilution of 1:40 is considered positive, and a fourfold increase in titer after one week has diagnostic value. It is currently believed that the detection of nuclear protein antibodies is beneficial for early diagnosis, while the detection of G2 antibodies is beneficial for prognosis. Recent foreign research has shown that an immunochromatographic rapid test using recombinant nuclear protein (NP) as the antigen can detect the patient's IgM antibodies in 5 minutes, with both sensitivity and specificity of 100%.

　　(4) PCR technology: RT-PCR is used to detect Han tan virus RNA, which has high sensitivity and can be used for early diagnosis.

　　Imaging examinations

　　1. Liver function: Serum alanine aminotransferase (ALT) levels are elevated in about 50% of patients, and a small number of patients have increased serum bilirubin levels.

　　2. Electrocardiogram: Sinus bradycardia, conduction block, and other arrhythmias and myocardial damage may be present. In addition, T waves become tall and pointed during hyperkalemia, and U waves appear during hypokalemia.

　　3. Intraocular pressure and fundus: Some patients have increased intraocular pressure, and those with significantly increased intraocular pressure often indicate severe illness. Patients with cerebral edema may show papilledema and venous congestion and dilation.

　　4. Chest X-ray: Approximately 30% of patients have pulmonary edema and congestion, and about 20% of patients show pleural effusion and pleurisy.

　　Dietary health care for hemorrhagic fever with renal syndrome

　　Diet during the high fever phase: Due to high body temperature, excessive sweating, and increased metabolism, patients in the high fever phase have a significant consumption of the body. Therefore, it is recommended to provide a nutritious and easily digestible semi-liquid or liquid diet rich in calories, vitamins, and high-quality protein. Examples include milk, soy milk, red bean rice porridge, lotus seed soup, natural juice, lotus root starch, egg soup, noodles, and instant noodles. The method of eating small meals frequently should be adopted to avoid increasing the burden on the gastrointestinal tract and causing indigestion. It is advisable to encourage patients to drink more water and eat more fruit to facilitate the excretion of toxins and increase the intake of vitamins to meet the body's needs. It is recommended to eat a low-salt diet, as excessive salt intake can worsen tissue edema and renal burden, leading to deterioration of the condition.

　　(One) Treatment

　　The treatment of this disease is mainly based on comprehensive therapy, with early antiviral treatment and symptomatic treatment for pathophysiological conditions in the middle and late stages. 'Three early and one local' treatment principle still applies. That is, early detection, early rest, early treatment, and local treatment. Attention should be paid to the prevention and treatment of shock, renal failure, and hemorrhage during treatment.

　　1. During the fever phase, the principle of treatment is: antiviral, alleviate exudation, improve toxic symptoms, and prevent DIC.

　　(1) Antiviral treatment: For patients within 4 days of onset, ribavirin 1g/d can be administered intravenously in 10% glucose injection for 3-5 days for antiviral treatment. Based on our experience and that of Xi'an Medical University, the ribavirin treatment group is significantly superior to the control group in terms of fever reduction, disappearance of urinary protein, platelet increase, and recovery. In addition, we conducted granulocyte Han tan virus antigen detection and found that 3 days after the application of ribavirin, the Han tan virus antigen in granulocytes was significantly lower than that in the control group. This indicates that early treatment with ribavirin can suppress the virus, alleviate the condition, and shorten the course of the disease.

　　(2) To alleviate exudation: Early bed rest should be recommended, and rutin, vitamin C, and other substances can be administered to reduce vascular permeability. Approximately 1000ml of balanced salt injection per day can be infused. For patients with high fever, excessive sweating, vomiting, or diarrhea, appropriate increases can be made. During the late stage of fever, 20% mannitol injection of 125-250ml can be administered to increase plasma osmotic pressure, alleviate exudation, and reduce edema.

　　(3) Improvement of toxic symptoms: High fever should be treated primarily with physical cooling. Avoid using strong diaphoresis antipyretic drugs to prevent further loss of blood volume due to excessive sweating. For patients with severe toxic symptoms, dexamethasone 5-10mg can be given intravenously. For those with frequent vomiting, 10mg of metoclopramide injection can be given intramuscularly.

　　(4) Prevention of DIC: Give 500ml of dextran 40 glucose injection or 40-60g/d of salvia miltiorrhiza injection intravenously to reduce blood viscosity. For patients with severe high fever, toxic symptoms, and severe exudation, regular detection of coagulation time should be performed. Tube method within 3 minutes or activated partial thromboplastin time (APTT) within 34s indicates a hypercoagulable state, and small-dose heparin anticoagulation can be given, generally 0.5-1mg/kg body weight, once every 6-12 hours, and anticoagulation time should be tested before re-administration. If the tube method coagulation time is >25min, it should be paused for one time. The course of treatment is 1-3 days.

　　2. Hypotension shock phase Treatment principle: Active resuscitation, attention to acid-base correction.

　　(1) Resuscitation of blood volume: It should be early, rapid, and appropriate. That is, when the tendency of hypotension occurs, it should be resuscitated early. It should be appropriate to avoid over-infusion of fluid causing pulmonary edema or heart failure. The fluid should be crystalloid and colloidal combined, mainly balanced salt, and it is forbidden to simply infuse glucose injection. Because the glucose infused into the body is oxidized into a hypotonic water solution, which quickly penetrates through the damaged blood vessels into the surrounding tissues, and cannot achieve the purpose of resuscitation. The electrolytes, acid-base balance, and osmotic pressure contained in the balanced salt solution are similar to those in the extracellular fluid of the human body, which is conducive to the balance of electrolytes and acid-base in the body. The commonly used compound sodium acetate injection contains 5.85g of sodium chloride, 0.33g of calcium chloride, 6.12g of sodium acetate, and 0.3g of potassium chloride per liter, which contains 145mmol/L of sodium, 4mmol/L of potassium, 108.5mmol/L of chloride, and 2.25mmoL/L of calcium.

　　According to our experience, for patients with severe shock, the use of double isotonic balanced salt solution (i.e., each liter of various electrolytes content is doubled) can achieve the purpose of rapid resuscitation. This is because after the infusion of hypertonic fluid, the extracellular fluid渗出于组织的体液回流血管内，thus achieving rapid expansion of blood volume. Colloid solutions commonly used include dextran 40, mannitol, plasma, and human serum albumin. The osmotic pressure of 10% dextran 40 is 1.5 times that of plasma, in addition to the expansion of blood volume, it also has the effect of preventing red blood cells and platelets from aggregating on the vascular wall, thus improving the microcirculation. The infusion volume should not exceed 1000ml/d, otherwise it is easy to cause bleeding. 20% mannitol injection solution is a hypertonic solution that can produce a significant expansion of blood volume. For severe or refractory shock, due to the large amount of plasma extravasation, it is advisable to supplement plasma or human serum albumin. However, due to blood hypercoagulability in this period, it is not advisable to use whole blood.

　　Resuscitation method: When hypotension occurs, isotonic balanced salt injection solution can be infused. If marked shock occurs, it is advisable to rapidly intravenously drip or inject double isotonic balanced salt injection solution or 20% mannitol injection solution, and maintain with dextran 40 or isotonic balanced salt solution after blood pressure rises. For severe shock, appropriate blood products should be supplemented. During resuscitation, blood pressure changes should be closely observed, and fluid infusion should be maintained for more than 24 hours after blood pressure returns to normal.

　　(2) Correct acidosis: Insufficient blood perfusion of tissues and organs caused by shock leads to impaired oxidative processes, increased lactic acid formation, and metabolic acidosis. If acid correction is not performed, it is easy to induce DIC, and it can reduce myocardial contractility and the responsiveness of blood vessels to vasoactive substances, which is not conducive to the correction of shock. Acid correction is mainly done with 5% sodium bicarbonate injection, which can be supplemented in batches based on the results of carbon dioxide binding power, or 60-80ml per time, 1-4 times per day according to the condition. Since the osmotic pressure of 5% sodium bicarbonate injection is four times that of plasma, it not only corrects acidosis but also has a volume expansion effect.

　　(3) Application of vasoactive drugs and renal cortical hormones: After fluid replacement and acid correction, hemoglobin has returned to normal, but blood pressure is still unstable. Vasoactive drugs such as dopamine 100-200mg/L can be administered intravenously, which has the effects of dilating visceral vessels and enhancing myocardial contraction. Anisodamine has the effect of dilating microvessels and relieving vascular spasm, and can be administered intravenously at a dose of 0.3-0.5mg/kg. Adrenal cortical hormones have the effects of maintaining vascular integrity, reducing extravasation, reducing peripheral vascular resistance, improving microcirculation, and stabilizing cell membranes and lysosomes, reducing the damage to organ parenchymal cells caused by shock. Dexamethasone 10-20mg is commonly used and administered intravenously.

　　3. Oliguria phase: The treatment principle is 'stabilize, promote, guide, and permeate'. That is, stabilize the internal environment of the body, promote diuresis, catharsis, and dialysis treatment.

　　(1) Stabilize the internal environment of the body:

　　Maintain water and electrolyte balance: Due to the overlap of oliguria phase and shock phase in some patients, early oliguria needs to be distinguished from pre-renal oliguria caused by shock. If the urine specific gravity is greater than 1.20 and the sodium concentration is 10:1, consider pre-renal oliguria. Electrolyte solutions of 500-1000ml can be infused, and the increase in urine volume should be observed. 20% mannitol injection of 100-125ml can also be administered by injection, and the urine volume should be observed for 3 hours. If the urine volume does not exceed 100ml, it is considered oliguria caused by renal parenchymal damage, and the input volume should be strictly controlled. The daily fluid intake should be the urine output and vomiting volume of the previous day plus 500-700ml. The main electrolyte disorder during oliguria is hyperkalemia, so potassium salts should not be supplemented, but a few patients may have hypokalemia. Therefore, appropriate potassium supplementation should be based on the results of blood potassium and electrocardiogram.

　　Reduce protein catabolism and control azotemia: High carbohydrate, high vitamin, and low protein diet should be provided. For those who cannot eat, intravenous infusion of glucose 200-300g/d can be given, and insulin can be added in appropriate amounts. Since the volume of infusion needs to be controlled, glucose should be used in a 20%-25% hypertonic solution.

　　Maintain acid-base balance: Metabolic acidosis is commonly accompanied by this period, so 5% sodium bicarbonate injection should be used to correct acidosis based on the results of carbon dioxide binding power. When carbon dioxide binding power test cannot be performed, 50-80ml of 5% sodium bicarbonate injection can be administered intravenously for infusion. If deep and rapid Kussmaul respiration persists after acid correction, continued correction of acidosis is required.

　　(2) Promoting diuresis: One of the reasons for oliguria in this disease is the compression of renal tubules by interstitial edema of the kidney, so in the early stage of oliguria, 20% mannitol injection 125ml can be administered intravenously to reduce interstitial edema of the kidney. If the diuretic effect is significant after administration, it can be repeated once, but it is not advisable to use it for a long time in large quantities. The commonly used diuretic drug is furosemide, which can start with a small dose and gradually increase the dose to 100-300mg per dose, administered intravenously. If the effect is not significant, the dose can be appropriately increased, and repeated every 4-6 hours. Vasodilators such as phentolamine 10mg or anisodamine 10-20mg can also be used for intravenous infusion, twice or three times a day, and propranolol can be used orally in the early stage of oliguria.

　　(3) Laxative and bloodletting therapy: To prevent high blood volume syndrome and hyperkalemia, laxative therapy can be performed to excrete excess water and potassium ions from the body through the intestines, but it must be done without gastrointestinal bleeding. Mannitol 25g, twice or three times a day, is commonly used, taken orally; or 40ml of 50% magnesium sulfate solution or 10-30g of rhubarb decocted in water, twice or three times a day, taken orally. Bloodletting therapy is now rarely used, and for patients with oliguria and high blood volume syndrome resulting in pulmonary edema and heart failure, bloodletting of 300-400ml can be performed.

　　(4) Dialysis therapy: Currently, peritoneal dialysis and hemodialysis are commonly used. The former, due to the improvement of dialysis catheters, currently uses ringed silicone dialysis catheters, which can prevent peritoneal infection caused by unstable catheter fixation and is easy to perform, suitable for grassroots units. The latter requires special equipment of an artificial kidney.

　　①Indications for dialysis therapy: Patients with oliguria lasting for more than 4 days or anuria for more than 24 hours, and one of the following conditions: A. Urea nitrogen > 28.56mmol/L; B. High catabolic state, with an increase in urea nitrogen of more than 7.14mmol/L per day. C. Blood potassium > 6mmol/L. ECG shows a tall T wave indicating hyperkalemia; D. High blood volume syndrome or accompanied by pulmonary edema; E. Severe restlessness or accompanied by cerebral edema.

　　②Peritoneal dialysis is based on the principle that the peritoneum is a semi-permeable membrane with diffusion and osmosis functions, which can remove nitrogenous waste and other waste products from the body: A. Incision: An incision 3-5 cm below the navel is made and a catheter is inserted; B. Adjustment of dialysis fluid composition: The commonly used dialysis fluid contains 5.6g of sodium chloride, 0.26g of calcium chloride, 0.15g of magnesium chloride, 5g of sodium lactate, and 15g of glucose per liter, with an osmolality of 364mmol/L. To prevent infection, 40,000U of gentamicin can be added to each liter of dialysis fluid. For patients with high blood volume syndrome, pulmonary edema, or cerebral edema, 40-45ml of 5% glucose injection can be added to each liter of dialysis fluid for dehydration; C. Dialysis fluid infusion: In winter and spring, the dialysis fluid needs to be heated to 37.5-38°C, infused 1000ml at a time, and released after 40 minutes, with 7-8 infusions per day; D. Observation: Pay attention to the body temperature, abdominal tenderness, and the color of the dialysis fluid and blood urea nitrogen. If the dialysis fluid released from the peritoneum is cloudy and contains a high protein content, to prevent fibrin from blocking the catheter, 50mg of heparin can be added to each liter of dialysis fluid.

　　③ Hemodialysis: Hemodialysis is performed every 2-3 days according to blood urea nitrogen levels, for 5-6 hours each time. Termination time of dialysis: dialysis can be stopped when urine output reaches more than 2000ml/d, blood urea nitrogen decreases, and hyperhydration syndrome or cerebral edema improves.

　　4. Treatment principles for polyuria phase The treatment during the transition period and the early stage of polyuria is the same as that during oliguria. The main treatment for the late stage of polyuria is to maintain water and electrolyte balance and prevent secondary infection.

　　(1) Maintenance of water and electrolyte balance: Provide semi-liquid foods and potassium-containing foods. Water replacement is mainly oral, and intravenous injection can be used for those who cannot eat.

　　(2) Prevention and treatment of secondary infection: Due to decreased immune function, respiratory and urinary tract infections are prone to occur during this period, so attention should be paid to oral hygiene, and indoor air disinfection should be carried out when necessary. After infection occurs, timely diagnosis and treatment should be given, and antibiotics with toxic effects on the kidneys should be avoided.

　　5. Recovery period Treatment principles are to supplement nutrition and gradually resume work. After discharge, rest for 1-2 months. Regularly review renal function, blood pressure, and pituitary function. If there are abnormalities, treatment should be given in a timely manner.

　　6. Treatment of complications

　　(1) Gastrointestinal bleeding: Pay attention to etiological treatment. If it is in the consumptive coagulopathy phase of disseminated intravascular coagulation (DIC), it is advisable to supplement coagulation factors and platelets, and cold sediment containing coagulation factors and platelet suspension can be administered. If it is in the hyperfibrinolysis phase of DIC, N-acetylcysteine 1g or aminomethylbenzoic acid 200-400mg can be used for intravenous infusion, twice or three times a day. If the bleeding is caused by increased heparin-like substances, then use protamine sulfate (protamine) 50-100mg per dose, injected slowly into the vein once a day or twice a day, or phenazopyridine 3-5mg/(kg·d) can be used orally or intravenously. Local treatment can be applied with thrombin 4000U diluted with 100ml of physiological saline for oral administration, twice or three times a day.

　　(2) Complications of central nervous system: Apply diazepam 10-20mg per dose, intravenous injection or sodium amytal 0.2-0.4g diluted with physiological saline to 20ml for intravenous injection when convulsions occur. Intracranial hypertension caused by cerebral edema or intracranial hemorrhage should be treated with mannitol 1-2g/kg body weight, intravenous bolus injection, once every 4-6 hours. During oliguria, mannitol is not recommended, and 10% glycerol saline 0.5-1.0g/kg body weight can be used for intravenous infusion, which can maintain the effect of reducing intracranial pressure for 3-4 hours. Avoid excessive dosage or rapid infusion to prevent hemolysis or renal damage. Dialysis treatment may be necessary, and hyperosmotic dialysis fluid should be used for dehydration.

　　(3) ARDS: Renal cortical hormones can reduce vascular permeability, reduce pulmonary exudation, promote the synthesis and secretion of pulmonary alveolar surface substances, inhibit the synthesis and release of histamine, 5-hydroxytryptamine, and slow-reacting substances, relieve bronchospasm, and are generally used at a dose of 100-250mg/d, orally, or dexamethasone 20-30mg, once every 8 hours, intravenously. In addition, water intake should be restricted and high-frequency ventilation or the use of a ventilator for artificial end-expiratory positive pressure breathing (PEEP) should be performed. The ventilator should be closely coordinated with oxygen therapy to reduce the workload on the heart. The application of the ventilator is only to relieve respiratory failure and win time for ARDS treatment. Recently, there have been reports that extracorporeal membrane oxygenation (ECMO) is used to treat ARDS and has achieved good effects.

　　(4) Heart failure pulmonary edema: Fluid infusion should be stopped or controlled, and digoxin (cedilanide) should be used for cardiotonic, diazepam for sedation, as well as vasodilators and diuretic drugs. If oliguria or anuria occurs, catharsis or dialysis treatment should be performed.

　　(5) Surgical suture for spontaneous renal rupture.

　　(6) Hyperosmolar Nonketotic Coma: During the hypotensive shock phase, 0.45% hypotonic saline should be supplemented, and human serum albumin or plasma should be supplemented to maintain blood volume. In addition, insulin should be used to lower blood sugar, and routine fluid replacement should be performed after the plasma osmolality decreases to 330mmol/L. During the polyuria phase, in addition to the use of hypotonic solutions and insulin, potassium supplementation should be noted.

　　(II) Prognosis

　　The mortality rate of this disease is related to the severity of the disease type, the timing of treatment, and whether the measures are correct. In recent years, with the improvement of early diagnosis and treatment measures, the mortality rate has decreased from 10% to below 5%. It is generally believed in China that the mortality rate of Hantavirus infection is higher than that of Seoul virus infection. The mortality rate of severe patients is still relatively high. The main causes of death are shock, uremia, pulmonary edema, and hemorrhage (mainly cerebral hemorrhage and pulmonary hemorrhage, etc.). Due to appropriate treatment measures, the number of deaths due to shock, uremia, and pulmonary edema has gradually decreased, while the number of deaths due to hemorrhage has increased relatively. Chronic renal function damage, hypertension, or hypopituitarism may occur after the recovery period of patients with this disease, indicating poor prognosis.