OVERVIEW
Hantavirus pulmonary syndrome (HPS) is caused by infection with Sinnabar virus (SNV) and its related hantaviruses. A syndrome characterized by pulmonary capillary leakage and cardiovascular involvement, it is also known as hantavirus cardiopulmonary syndrome (HCPS). The disease has occurred in at least 30 states in the United States, and in recent years cases have been reported in Germany and Sweden in Europe. It occurs throughout the year, but is most prevalent in spring and summer, with a high incidence in years of heavy rainfall and cooler climates. The disease has an incubation period of several days to 6 weeks or longer. There is no HPS found in China, but China is a high prevalence of epidemic hemorrhagic fever, with the emergence of HPS in the continent of Europe outside the Americas, and into the year in our country appeared in the severe acute respiratory syndrome (SARS) and the identification of HPS also appears to be particularly important, requires a high degree of vigilance.
Etiology
Hantavirus pulmonary syndrome (HPS) is caused by infection with Sinopah virus (SNV) and its related hantaviruses.
1. Pathogenesis and epidemiology
(1) Pathogen SNV is a virus belonging to the genus Hantavirus, which uses deer mice as hosts.
(2) Transmission is unknown. Like other hantaviruses, SNV may be excreted in the feces, urine and saliva of rodents and inhaled as aerosols or particles.
(3) Prevalence and influencing factors The disease has occurred in at least 30 states in the United States, and in recent years cases have been reported in Germany and Sweden in Europe. Increased contact between humans and rodents is one of the important influencing factors, so the occupational risk is causing concern.
2. Pathogenesis and pathophysiology
The pathogenesis is not clear. CD8+ and CD4+ cytotoxic T-lymphocytes that specifically recognize hantavirus can be isolated from the patient’s blood, and the immune response of granulocytes to the infected cells leads to increased permeability of alveolar capillaries. The lungs are the primary target organ and clinically present with intra-alveolar edema and hypoxemia. Rapidly developing pulmonary edema and shock due to myocardial depression and hypovolemia are the two main pathophysiologic changes that threaten the lives of patients with HPS.
Symptoms
The typical course of HPS is divided into 3 phases: prodromal, cardiopulmonary, and recovery.
1. Prodromal stage
The onset of the disease is often acute, with prodromal symptoms such as chills, fever, myalgia, headache, malaise and other toxic symptoms. Can also be accompanied by nausea, vomiting, diarrhea, abdominal pain and other gastrointestinal symptoms. Fever is generally 38 ℃ ~ 40 ℃, the above symptoms last for 12 hours, an average of 3 ~ 6 days.
2. Cardiopulmonary stage
Most of the 2 ~ 3 days after the rapid emergence of cough, shortness of breath and respiratory distress and enter the respiratory failure period, this period for non-cardiogenic pulmonary edema. Physical examination shows that the respiratory rate increases, the heart rate increases, coarse or fine wet rales can be heard in the lungs, and a few patients have pleural effusion or pericardial effusion. In severe cases, hypotension, shock, heart failure, and arrhythmias such as sinus bradycardia or sinus tachycardia may occur. Only a few patients are found to have lid conjunctival congestion, bulbar conjunctival edema, skin and mucous membrane hemorrhagic spots or hemorrhagic spots.
3.Recovery period
Patients who can pass the respiratory failure stage gradually enter the recovery stage, at this time the respiration is stable, the hypoxia is corrected, but a small number of patients can still be seen in the persistence of low-grade fever, and the physical strength still has some time to recover. However, some patients do not have pulmonary syndrome.
Examination
1. Laboratory examination
Most patients with this disease have elevated white blood cell counts, up to (30-65)×109/L. Neutrophils are obviously elevated, with leftward shifting of the nucleus, which may appear as immunoblast-type lymphocytes, late juvenile granulocytes and/or mesophilic granulocytes, and heterogeneous lymphocytes are common; platelets are obviously reduced, and some patients have hemoconcentration, with elevation of erythrocytes and hemoglobin and increase in hematocrit.
2. Other auxiliary examinations
(1) Patients with renal damage may have urinary protein and microscopic hematuria, and urinary protein is usually ++.
(2) Blood biochemical examination: ALT and AST are elevated and hypoproteinemia, in addition, LDH and creatine kinase are often elevated, urea nitrogen and creatinine are elevated in patients with renal damage, and a few patients have metabolic acidosis.
(3) Arterial catheterization examination, low pulmonary artery wedge pressure and markedly reduced cardiac index suggest non-cardiogenic pulmonary edema.
(4) X-ray examination: infiltration shadow can be seen in the interstitium of both lungs, or infiltration shadow can be seen in both interstitium and alveoli, and pleural effusion and pericardial effusion can be seen in some patients.
(5) Bronchoscopy found that the airway was normal, no bronchial mucosal damage was found, and erythema was seen in the airway of a few patients. Measurement of total protein, clear protein and lactate dehydrogenase in the endotracheal aspirate is significantly higher, even reaching or exceeding the serum level.
3. Coagulation function examination
Prolongation of whole blood partial thromboplastin time (WBPTT) and prothrombin time can be seen, and fibrin degradation products are elevated in a few patients, but fibrinogen is normal.
Diagnosis.
A history of rodent exposure, typical clinical course, signs and symptoms of cardiopulmonary involvement, physical signs and hematologic changes contribute to the diagnosis of the disease.
Differential Diagnosis
HPS needs to be differentiated from various types of bacterial and viral pneumonia.
Treatment
Specific treatment is lacking. Ribavirin can be used early in the course of the disease; it is ineffective when used after entering the cardiopulmonary phase. Current treatments are supportive, especially respiratory and circulatory support. Oxygen therapy and mechanical ventilation are routinely used.