Symptoms of hemolytic-uremic syndrome
Last reviewed: 23.04.2024
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Hemolytic-uremic syndrome in young children
Complicates the course of the infectious process caused by a variety of viral and bacterial agents; is described as a complication of vaccinations against smallpox, diphtheria, measles, tetanus and poliomyelitis.
Symptoms of hemolytic-uremic syndrome
During the syndrome, three periods are distinguished: prodromal, peak period and recovery period.
The prodromal period begins with symptoms of a lesion of the gastrointestinal tract or upper respiratory tract. They are joined by neurological disorders of varying degrees, peripheral blood flow insufficiency and metabolic disturbances. Pallor of the skin and mucous membranes are noted, scleras are often injected, in the region of the nose, eyelids, and lips there is a pasty. At the end of the prodromal period, which lasts from two to seven days, there is an oligoanuria.
The peak period is characterized by three leading syndromes: hemolytic anemia, disseminated intravascular coagulation with thrombocytopenia, acute renal failure.
Skin and mucous become pale-icteric. There is a hemorrhagic syndrome: single or repeated nasal bleeding, petechial rash and ecchymosis on the skin.
For the oligoanuric stage of acute renal failure, this syndrome is characterized by the absence of edema, since there are significant fluid losses with stools and by perspiration.
Neurological disorders are diverse and are detected in half of the children. Early clinical signs of CNS damage are a change in attitudes toward others, inadequate emotional responses, hyperexcitability, anxiety, which in a few hours, less often days, are replaced by progressive lethargy, possibly the development of coma. Muscular twitching, myoclonic cramps and hyperreflexia indicate the need for emergency dialysis before the appearance of much more serious signs of CNS involvement in hemolytic-uremic syndrome. Meningeal symptoms are absent, in some patients, stiff neck and positive Kernig symptom are noted. The pressure of the cerebrospinal fluid can be increased, the protein content is somewhat increased, but the absence of pleocytosis and normal sugar content in the cerebrospinal fluid help differentiate hemolytic-uremic syndrome from meningitis. Dysfunction of the central nervous system may be secondary to uremic intoxication; in some patients they are caused by diffuse capillary thrombosis of the brain vessels or caused by a virus that is equally tropic both to the nervous and to the kidney tissue.
Changes in the cardiovascular system are manifested by tachycardia, muffled heart tones, systolic murmur, extrasystoles are possible. The degree of myocardial damage corresponds to the severity of hyperkalemia. Arterial pressure, lowered in the first period, for 2-3 days of clinical manifestations increases. Persistent arterial hypertension is prognostically an unfavorable sign and indirectly indicates a severe irreversible necrosis of the renal cortex. Arterial hypertension and hyperkalemia, as a rule, lead to heart failure. With early use of dialysis, pericarditis is rare.
Corresponding to the severity of metabolic disorders and acidosis, dyspnea appears. Above the lungs they listen to hard breathing, less often small bubbling rales. If the onset of the syndrome occurred against the background of acute respiratory viral infection, pneumonia is usually diagnosed. A frequent complication of hyperhydration is pulmonary edema with an x-ray picture of the darkening of the basal zone in the form of a butterfly silhouette with a peripheral zone free from dimming.
Oligoanuria is partially compensated by the activity of other organs and systems, primarily by strengthening the function of the glandular apparatus of the mucous membrane of the gastrointestinal tract and sweat glands. Together with gastric and intestinal juices, 1.5-2 g of urea per day are released into the intestinal lumen of children. Increased accumulation of nitrogen metabolism products and electrolyte disorders increase the symptoms of gastroenteritis. Paresis of the intestine can develop. However, this complication occurs more often in the polyuric phase and is associated with hypokalemia. Most patients are diagnosed with hepatomegaly, less often with a simultaneous increase in the spleen.
With the appropriate pathogenetic therapy, the oligo-anuric stage passes into the polyuric stage, which is no less dangerous for the patient, since the child's organism catastrophically loses water and electrolytes.
The severity and duration of this phase depend on the depth of kidney damage and the rate of regeneration of tubular epithelium cells. The duration of the polyuric phase is 3-4 weeks. Already at the end of the first week of the polyuric stage, hypera-isotomy disappears and the water-electrolyte balance is restored.
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