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The names of diseases hemolytic uremic syndrome (kidney medicine) disease disease is more common in infants and young children Introduction. Cause is unknown, some children prior to the onset of fever or viral, it may be associated with infection or immune complex mediated by. Similar clinical manifestations and TPP, with fever, thrombocytopenia, microvascular hemolytic anemia, hypertension and acute renal failure, neurological symptoms are not common. But micro-hemolytic and capillary damage is mainly confined to the kidney, can be seen as the focal type of TPP. No effective treatment, acute renal failure may be given dialysis, some cases may be spontaneous remission. Clinical manifestations 1. Prodromal manifestations: diarrhea, abdominal pain, vomiting and loss of appetite for several days; 2. Acute microvascular hemolytic anemia; 3. Disseminated intravascular coagulation, showing extensive hemorrhagic tendency; 4. Acute renal failure, oliguria performance no urine; 5. Other: If the performance of the circulatory system (hypertension, arrhythmia, heart failure), nervous system (drowsiness, convulsions, coma). Diagnosis is based . Evidence of hemolytic anemia: severe anemia in a short time, reticulocyte 3% -5%, lactate dehydrogenase increased; 2. Thrombocytopenic evidence: systemic multi-site bleeding, platelet count more than <50 10 9 th / L; 3. progressive renal failure: oliguria, anuria, blood urea nitrogen, serum creatinine increased; 4. coagulopathy: coagulation


time, increased fibrin degradation products; 5. Kidney Biopsy: Renal microvascular thrombosis. Therapy treatment principles: 1. Symptomatic treatment and supportive care; 2. To correct water-electrolyte and acid-base metabolism imbalance; 3. Blood purification therapy; 4. Anticoagulation therapy. Medicine principles: 1. In general, first consider the application of medication to be confined "A"; 2. Poor efficacy, or patient serious condition, and then consider the use of medication to be confined "C". Efficacy Evaluation: 1. Healing: hemolysis, bleeding stopped, reticulocyte 0.5-1.5%, urine examination was normal, with normal renal function; 2. Better: stop the bleeding, hemolysis greatly improved, urine normal, renal function recovered; 3. healed: bleeding, hemolysis is not controlled, renal function did not improve or become chronic renal failure. Common sense prevention of clinical disease often critical illness and, if found in patients with progressive anemia, acute renal failure, renal biopsy must be done against the clock to a regular hospital and blood purification timely rescue.
Severity of the disease as acute disease. Fibrin have loose cords calm in the many small blood vessels, damage of platelets and red blood cell flow through the cause of thrombocytopenia and microangiopathic hemolytic anemia. Among the many small blood clots caused by platelet consumption is also thrombocytopenia. Although thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome HUS generally considered to be different, but the only difference is the degree of renal failure, the differences in diagnosis and treatment are the same. Symptoms , signs and diagnosis of TTP-HUS is a potentially fatal acute disease, characterized by: (1), severe thrombocytopenia, (2), see the fragmentation of blood smears in the red blood cell (helmet-shaped cells, red triangle, the shape distortion of red blood cells) with evidence of hemolysis (Hb level lower, immature red blood cells increased, the number of reticulated cells increased, increased levels of serum lactate dehydrogenase), (3) acute renal failure, (4) fever, (5) Multi-dirty There were mixed control of ischemic injury. Clinical manifestations include central nervous system symptoms (blurred consciousness, and coma); varying degrees of jaundice (due to hemolysis and also that liver cell damage, direct and indirect bilirubin may go high). proteinuria, hematuria and acute renal failure. may also have abdominal pain, and heart rate changes induced myocardial damage. These symptoms involving multiple organ-specific vascular pathological damage. This multi-organ disease damage - mild platelet - fibrin thrombus (blood vessels in and around the no as vasculitis performance of granulocyte infiltration) is mainly confined to the small arteries and capillaries junction. This is called thrombotic microangiopathy. In addition to intestinal bleeding associated with E. coli O157 and Shiga toxin and the epidemic of children bacteria (typically referred to as HUS) often spontaneous remission does not need outside of plasma exchange, TTP-HUS is difficult to distinguish the various clinical syndromes. Although the some patients have a clear etiology (such as quinine allergy) or concomitant conditions (such as pregnancy), but suddenly and spontaneously in most patients with no obvious cause of seizures. by these diseases and other diseases (such as scleroderma, malignant Hypertension, acute renal graft rejection the same) in the same biopsy to prove the existence of thrombotic microangiopathy, which emphasizes the TTP-HUS and related syndromes (such as pre-eclampsia) is impossible to distinguish. prognosis and treatment TTP- HUS epidemic than other children, almost always fatal without treatment of .70 years of plasma exchange therapy was introduced significant changes in the prognosis of this syndrome. At present 80% of the patients were fully recovered. continuing daily plasma exchange treatment until evidence of disease activity disappeared, treatment may take several days to several weeks. generally given corticosteroids. some patients the use of antiplatelet drugs (such as a large dose of dipyridamole and aspirin), but the effects are questionable. must be carefully followed up on a few patients years; most patients TTT-HUS is only a one-time attack. However, relapse can also be repeated, this time to be re-plasma exchange therapy.


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