Symptoms of hemolytic uremic syndrome

Hemolytic uremic syndrome in young children

Complicates the course of the infectious process caused by various viral and bacterial agents; described as a complication of vaccinations against smallpox, diphtheria, measles, tetanus and poliomyelitis.

Symptoms of hemolytic uremic syndrome

During the course of the syndrome, three periods are distinguished: prodromal, acute period, and recovery period.

The prodromal period begins with symptoms of damage to the gastrointestinal tract or upper respiratory tract. They are accompanied by neurological disorders of varying degrees, insufficiency of peripheral blood flow and metabolic disorders. Paleness of the skin and mucous membranes is noted, the sclera is often injected, pastosity appears in the area of the nose, eyelids, lips. At the end of the prodromal period, which lasts from two to seven days, oliguria occurs.

The peak period is characterized by three leading syndromes: hemolytic anemia, disseminated intravascular coagulation with thrombocytopenia, and acute renal failure.

The skin and mucous membranes become pale and icteric. Hemorrhagic syndrome appears: single or repeated nosebleeds, petechial rash and ecchymosis on the skin.

The oligoanuric stage of acute renal failure in this syndrome is characterized by the absence of edema, since there is significant fluid loss with stool and through perspiration.

Neurological disorders are varied and are detected in half of the children. Early clinical signs of CNS damage are changes in attitude towards others, inadequate emotional reactions, hyperexcitability, anxiety, which after several hours, less often days, are replaced by progressive lethargy, and coma may develop. Muscle twitching, myoclonic seizures, and hyperreflexia indicate the need for emergency dialysis before the appearance of much more serious signs of CNS damage in hemolytic uremic syndrome. Meningeal symptoms are absent, some patients have stiff neck and a positive Kernig's sign. Cerebrospinal fluid pressure may be elevated, protein content may be slightly increased, but the absence of pleocytosis and normal sugar content in the cerebrospinal fluid help differentiate hemolytic uremic syndrome from meningitis. CNS dysfunction may be secondary to uremic intoxication; In some patients, they are caused by disseminated capillary thrombosis of the cerebral vessels or are caused by a virus that is equally tropic to both nervous and renal tissue.

Changes in the cardiovascular system are manifested by tachycardia, muffled heart sounds, systolic murmur, and possible extrasystoles. The degree of myocardial damage corresponds to the severity of hyperkalemia. Blood pressure, reduced in the first period, increases within 2-3 days of clinical manifestations. Persistent arterial hypertension is an unfavorable prognostic sign and indirectly indicates severe irreversible necrosis of the renal cortex. Arterial hypertension and hyperkalemia, as a rule, lead to heart failure. Pericarditis is rare with early use of dialysis.

According to the severity of metabolic disorders and acidosis, dyspnea appears. Hard breathing is heard over the lungs, less often - fine bubbling rales. If the onset of the syndrome occurred against the background of ARVI, then pneumonia is usually diagnosed. A frequent complication of hyperhydration is pulmonary edema with an X-ray picture of darkening of the root zone in the form of a butterfly silhouette with a peripheral zone free of darkening.

Oliguanuria is partially compensated by the activity of other organs and systems, primarily by increased function of the glandular apparatus of the gastrointestinal mucosa 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. Intestinal paresis may develop. However, this complication is more common in the polyuric phase and is associated with hypokalemia. Most patients have hepatomegaly, less often with a simultaneous enlargement of the spleen.

With appropriate pathogenetic therapy, the oligoanuric stage turns into a polyuric stage, which is no less dangerous for the patient, since the child’s body 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 epithelial cells. The duration of the polyuric phase is 3-4 weeks. Already at the end of the 1st week of the polyuric stage, hyperazotemia disappears and the water-electrolyte balance is restored.

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