Congestion of cheeks and upper chest

Introduction Epidemic hemorrhagic fever (EHF) is a natural epidemic disease caused by viruses. In 1982, the World Health Organization (WHO) named hemorrhagic fever with renal syndromes (HFRS). The main pathological changes of this disease are extensive damage of systemic small blood vessels and capillaries, body aches, flushing on the face and upper chest, bleeding on the skin combined with membrane congestion and edema, WBC abnormal lymph and urine protein (++). Clinically, it is characterized by fever, hypotension, hemorrhage, and kidney damage.

Cause

(1) Host animals and sources of infection: mainly small rodents, including Apodemus (mainly Apodemus agrarius), Rat genus (mainly Rattus norvegicus, Rat), Rat (brown back, red back) , voles (mainly oriental voles), hamsters (mainly black-line hamsters) and mouse genus (mute house mice, mice). China has detected more than 30 kinds of animals that can naturally carry the virus. In addition to rodents, some livestock also carry EHFV, including domestic cats, rabbits, dogs, pigs, etc., which proves multi-host. Most of these animals are carried by chance. Only a few mouse species have been proved to be the source of infection of the disease from epidemiology. Among them, Apodemus agrarius is the main host and source of infection for wild-type hemorrhagic fever, and Rattus norvegicus is urban. (Japan, North Korea) and the main source of infection of rat hemorrhagic fever in China, Dalin Apodemus is the main source of infection for hemorrhagic fever in forest areas of China. As for the epidemiological role of other rodents carrying the virus, further observation is needed.

(B) the route of transmission: the main spread is animal-derived, the virus can be discharged through the blood and saliva of the host animal, urine, and the direct transmission of the mouse to humans is an important way of human infection.

It is currently believed that the following pathways can cause hemorrhagic heat to spread:

1. Respiratory tract: The aerosol particles formed by the murine excretion containing the hemorrhagic fever virus contaminate the dust are infected through the respiratory tract.

2. Digestive tract: food and water contaminated by the excretion of rats with hemorrhagic fever virus, infected through the oral mucosa and gastrointestinal mucosa.

3. Contact transmission: bite by rats, rat excrement, secretion directly contact with damaged skin and mucous membranes.

4. Mother-to-child transmission: pregnant women can be infected with the fetus through the placenta after illness.

5. Insect-borne transmission: The parasitic mites of mice on the surface of the body can cause the spread of this disease.

(3) Susceptibility of the population: It is generally considered that the population is generally susceptible, and the rate of latent infection is low. The voles are mostly 3-4% or less; but the rate of recessive infection in the infected area is higher, with a report of 15%. Above, the incidence of young adults is high, and the incidence of secondary infections is rare. Serum-specific antibodies can be detected during the fever period after the disease, reaching a very high level from 1 to 2 weeks, and the antibody lasts for a long time.

an examination

Related inspection

Urine protein test (PRO) blood pressure

Clinical symptoms:

The oliguria period often overlaps with the hypotensive shock phase without significant boundaries. In the middle and the low blood pressure, oliguria can occur, and some people directly enter the oliguria period from the fever period, and the fever is manifested. Hypotension and oliguria overlap are often severe cases.

1. The appearance and duration of oliguria: generally on the 5th to 8th day of the disease, the 3rd day of the disease, and the 10th day of the night, lasting 2-5 days.

2, oliguria strength: 24h urine volume <1000ml for oliguria tendency, <500ml for oliguria, <50ml for auria, some cases of oliguria is not obvious, but there is azotemia, called "none Oliguria-induced renal failure."

3, clinical manifestations of oliguria: due to renal failure, renal excretion dysfunction, a large number of metabolites and fluid retention in the body, electrolyte imbalance, azotemia and / or uremia, acidosis, high blood volume syndrome Such as anorexia nausea, bloating, dizziness, headache, large skin ecchymosis, rapid breathing, weak myocardial contraction, decreased blood pressure, head pain during high blood volume, body toxic V filling, large pulse, high blood pressure, rising heart rate, Red blood cells, hemoglobin, and decreased blood pressure.

The incubation period is 5 to 46 days, usually 1 to 2 weeks. The disease typically has three main symptoms of fever, hemorrhage and kidney damage, as well as five clinical stages of fever, hypotension, oliguria, polyuria and recovery. In most cases, the clinical manifestations are not typical, or the performance in a certain period is outstanding, or the period is not obvious and the phenomenon is "overdue", or the first two or three periods overlap.

(A) fever period: mainly manifested as infectious viremia and symptoms caused by systemic capillary damage. Most of them suddenly have chills and fever, and the body temperature can reach 39 to 40 °C within 1 to 2 days. The heat type is mostly relaxation and retention, and generally lasts for 3 to 7 days. Symptoms of systemic poisoning, high fatigue, body aches, headaches and severe low back pain, eyelid pain, known as "three pains." Headache may be related to cerebral vasodilatation and congestion; low back pain is related to congestion and edema around the kidney; eyelid pain may be caused by edema around the eyeball. Gastrointestinal symptoms are also prominent, often with appetite, nausea, vomiting, abdominal pain and diarrhea. In severe cases, there may be drowsiness, irritability and slang. However, the symptoms of systemic poisoning have not been alleviated or worsened after the heat is reduced, which is different from the clinical features of other heat-induced diseases.

(B) hypotension period: mainly for the performance of plasma loss of hypovolemic shock.

Generally, on the 4th to 6th day of fever, when the body temperature starts to drop or shortly after the fever, the patient has hypotension, and the severe person suffers from shock. It can be combined with DIC, heart failure, water and electrolyte imbalance, clinical manifestation of heart rate, cold limbs, decreased urine output, irritability, unconsciousness, cyanosis at the lips and extremities, shortness of breath, and increased bleeding. This period generally lasts for 1 to 3 days, and severe cases can reach more than 6 days. And often due to heart and kidney failure caused by death, this period can also be invisible and quickly into the oliguria or polyuria.

(C) oliguria: There are often no obvious boundaries between oliguria and hypotension, and the two often overlap or follow each other, and there is no hypotension shock, from the fever period directly into the oliguria. 24 hours of urine less than 400ml for oliguria, less than 50ml for anuria. The main clinical manifestations of this period are azotemia and imbalance of water and electrolyte balance. It is also possible that a large amount of fluid accumulated in the interstitial space is returned to the blood circulation, so that a high blood volume syndrome occurs. This period begins on 6-8 days of illness, blood pressure rises, urine volume decreases sharply, and even urine closure occurs. In severe cases, membranous or hematuria occurs in the urine. In this period, there are often varying degrees of uremia, acidosis, and electrolyte imbalance (high potassium, low sodium, and hypocalcemia). With high blood volume syndrome, the pulse is full and powerful, venous engorgement, progressive hypertension and hemodilution. Severe cases can be associated with heart failure, pulmonary edema and cerebral edema. At the same time, the bleeding tendency is aggravated, and common skin ecchymoses and channel bleeding are common. This period generally lasts for 2-5 days. In severe cases, there is no urine for more than 1 week. The current weight is parallel with oliguria and azotemia.

Differential diagnosis

Cheeks are obviously invaginated: cheek depressions on both sides are one of the causes of distress. If the cheeks are sag, the sacral bulge can be seen. The two sag collapses, the small wrinkles can be seen on the cheeks and the corners of the mouth, the skin is dry, the skin color is yellow and white, and it is much older than the actual age.

Facial congestion is cherry red: due to systemic telangiectasia, increased vascular permeability, can be expressed as facial congestion, facial redness, cherry red, visible in oxide poisoning. According to the occupational history of inhaling a large amount of nitrogen oxides in a short period of time, the clinical manifestations of respiratory damage and chest x-ray signs, combined with blood gas analysis and on-site labor hygiene survey data, comprehensive analysis, and exclusion of similar diseases caused by other causes, Can be diagnosed.

The lips are severely congested in red: mucocutaneous lymph node syndrome (MCLS), also known as Kawasaki disease, is an acute febrile rash pediatric disease characterized by systemic vasculitis. In 1967, Japanese Kawasaki Fusuke doctor reported for the first time. Because this disease can cause serious cardiovascular disease, causing people to pay attention to it, the incidence has increased in recent years. In the hospitalized cases of rheumatic diseases in Beijing Children's Hospital in 1990, 67 cases of Kawasaki disease, 27 cases of rheumatic fever; the same information of 11 hospitals in other provinces and cities Kawasaki disease is twice as much as rheumatism. Obviously, Kawasaki disease has replaced rheumatic fever as one of the main causes of acquired heart disease in children in China. Kawasaki disease is currently considered to be an immune-mediated vasculitis that is temporarily included in the connective tissue disease.

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