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Diagnosis of hemolytic-uremic syndrome
Last reviewed: 23.04.2024
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The data of the clinical analysis of the blood depend on the period of the disease and the compensatory possibilities of the organism. In the period of height, normochromic hyperregenerative anemia of various severity is observed, morphologically marked pronounced anisocytosis of erythrocytes (micro- and macrocytosis), erythrocytes acquire distorted fragmented forms in the form of rods, triangles, eggshell discs with scalloped edges (fragmentocytosis). One of the most important signs is thrombocytopenia, the degree of which is equal to the severity of hemolytic crisis; in most patients, a decrease in the number of platelets can be significant. There is leukocytosis (20-60 x 109 / l) with a shift to the left up to metamyelocytes, promyelocytes, blast cells. A number of observations describe leukopenia. Sometimes there is eosinophilia (up to 8-25%).
The hemolytic nature of anemia is confirmed by an increase in total serum bilirubin (due to indirect bilirubin), a decrease in the content of haptoglobin, a significant increase in the level of free hemoglobin in plasma, hemoglobinuria.
Correspondingly, the severity of renal failure reveals a high content of residual nitrogen, urea and creatinine. The rate of increase in blood urea levels depends on the intensity of catabolic processes. Often the daily increase in urea ranges between 4.89-9.99 mmol / l, and creatinine 0.088-0.132 mmol / l. The increase in urea over 6.6 mmol / l is an indication for extracorporeal detoxification.
Often observed hypoalbuminemia (30,0-17,6 g / l), hypoalbuminemia below 25 g / l is an unfavorable prognostic factor in children of early age with hemolytic uremic syndrome in the background of intestinal infection.
Disorders of water-electrolyte metabolism are manifested by an increase in the concentration of intracellular electrolytes (potassium, magnesium, phosphates) in the blood and a decrease in the concentration of extracellular electrolytes (sodium and chlorine), which usually corresponds to the severity of dehydration due to profuse vomiting and diarrhea.
Hemocoagulation changes depend on the phase of the DIC syndrome. Hypercoagulation is accompanied by a shortening of the coagulation time of venous blood, recalcification time, an increase in thrombotest, a normal or slightly increased level of factors of the prothrombin complex. In the blood and urine, fibrin degradation products are identified; anticoagulant and fibrinolytic activity of blood are compensated.
In the phase of hypocoagulation, which is usually observed in the terminal period of the disease, due to the consumption of clotting factors, lengthening of clotting time, recalcification time, reduction of thrombotest, decrease of factors taking part in formation of active blood thromboplastin, factors of prothrombin complex and fibrinogen level are noted. Usually, these changes are accompanied by extensive hemorrhages at the injection site and severe bleeding from the respiratory or gastrointestinal tract.
In the analysis of urine, proteinuria, macro- or microhematuria are detected. In hemolytic anemia, urine acquires the color of dark beer due to hemoglobin. It is very characteristic for hemolytic-uremic syndrome is the detection of fibrin lumps in the urine. A loose slimy lump sized from corn grain to hazelnut white or slightly pink in color, floating in the urine, is of great diagnostic value, since it indicates the process of intravascular coagulation with the deposition of fibrin on the endothelium of capillary gland loops.
Pathological studies of patients who died from hemolytic-uremic syndrome, reveal varying degrees of kidney damage from a picture of acute microthrombotic glomerulonephritis to bilateral necrosis of the kidney cortex. Along with changes in the kidneys, a picture of disseminated vascular thrombosis (mostly of small caliber) is revealed in many internal organs, accompanied by hemorrhagic or ischemic infarcts. The severity of the lesions of the same organs varies in different patients with the identity of the clinical picture.
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