hemorrhagic shock and encephalopathy syndrome
Introduction
Introduction to hemorrhagic shock and encephalopathy syndrome Hemorrhagic shock and encephalopathy syndrome (HSES) is a rare condition characterized by severe shock, encephalopathy and other symptoms of an acute exacerbation in a previously healthy child, and results in death or extremely severe neurological damage. The onset is rapid, the mortality rate is high, and the survivors are prone to have serious neurological sequelae. It is characterized by sudden coma and convulsions, shock, BCD, watery diarrhea, metabolic acidosis, liver and kidney dysfunction. Hemorrhagic shock and encephalopathy syndrome occur mainly in infants between 3 and 8 months (mean age is 5 months), but it has also been reported to occur at 15 years of age. Most children have symptoms of prodromal fever, upper respiratory symptoms, vomiting and diarrhea. The main clinical features are acute onset encephalopathy (expressed as convulsions, coma and decreased muscle tone) and severe shock. Other common clinical features include high fever (up to 43.9 ° C, rectal temperature), diffuse intravascular coagulation, cerebral edema, blood in the stool, metabolic acidosis, elevated liver transaminase, acute renal failure, thrombocytopenia, and decreased hematocrit. Primary lung and heart muscle involvement is rare. basic knowledge The proportion of illness: 0.005%-0.008% Susceptible population: infants that occur between 3 and 8 months Mode of infection: non-infectious Complications: metabolic acidosis
Cause
Hemorrhagic shock and etiology of encephalopathy syndrome
The cause is still unclear, and more reports have detected rotavirus and parainfluenza virus. The medical community believes that HSES is an overheating injury caused by over-wrapping a child with fever. Although HSES is rare in the neonatal period, there is no consistent report of over-tightening. Other theories include reactions to enterotoxin, environmental toxicants, trypsin released by the pancreas or unidentified bacteria or viruses. Reports on increased plasma proteases and decreased plasma protease inhibitors. It is not known that this reduction is either primary (synthesis or release defects) or secondary (due to increased consumption or inactivation).
Allergic cerebral edema with cerebral palsy, focal hemorrhage or infarction in the cerebral cortex and other organs can be found. Other non-specific findings have been described, including spotted hepatocyte turbidity and degeneration, but no steatosis like Reye syndrome.
Prevention
Hemorrhagic shock and prevention of encephalopathy syndrome
The disease may have mild to severe motor dysfunction, and after a few months it is mostly sports degeneration and sequelae of epilepsy. Most of the cases (>60%) die, and 70% or more of the survivors have serious Nervous system sequelae.
Complication
Hemorrhagic shock and complications of encephalopathy syndrome Complications metabolic acidosis
There are mild to severe motor dysfunction, metabolic acidosis, and after a few months, most of them are sports degeneration and sequelae of epilepsy. Most of the cases (>60%) die, 70% or more of the survivors Severe neurological sequelae.
Symptom
Hemorrhagic shock and symptoms of encephalopathy syndrome Common symptoms Coma fever accompanied by abdominal pain, ... Hepatic tunica rupture watery stool convulsions convulsion shock low intracranial pressure syndrome
Most children have symptoms of prodromal fever, upper respiratory symptoms, vomiting and diarrhea. The main clinical features are acute onset encephalopathy (expressed as convulsions, coma and decreased muscle tone) and severe shock. Other common clinical features include high fever (up to 43.9 ° C, rectal temperature), diffuse intravascular coagulation, cerebral edema, blood in the stool, metabolic acidosis, elevated liver transaminase, acute renal failure, thrombocytopenia, and decreased hematocrit. Primary lung and heart muscle involvement is rare. Laboratory tests often show leukocytosis, hypoglycemia, hyperkalemia, but blood ammonia is normal. Both bacteriology and virus culture were negative.
Examine
Hemorrhagic shock and examination of encephalopathy syndrome
Test items: hemoglobin, platelets, ALT (alanine aminotransferase), AST (aspartate aminotransferase), PT (prothrombin time), APTT (white clay partial thrombin time), FDP (fibrinogen degradation product), pH, PCO2 , BUN (urea nitrogen), Cr (creatinine), lactic acid, EEG, head CT.
Diagnosis
Diagnostic identification of hemorrhagic shock and encephalopathy syndrome
The results of laboratory tests for elevated ALT and AST, hemoglobin, and thrombocytopenia are diagnostic conditions. Differential diagnosis includes septic shock, Reye syndrome, toxic shock syndrome, hemolytic uremic syndrome, heat stroke and viral hemorrhagic fever, Reye's syndrome and toxic shock, excluded according to their clinical course or laboratory performance.
The clinical features of HSES brain damage can be divided into two categories: fulminant and brain dysfunction. The former: into the coma within 24 hours after admission, frequent convulsions, significantly reduced muscle tone, accompanied by heart, lung, kidney, blood and other organ failure. Levin et al reported 25 cases (20 of them died); the vast majority of patients had reduced muscle tone after admission, while the convulsive status and coma time were greater than 24 h, the prognosis was poor. Ince et al reported 4 cases: convulsions were most frequent in the onset. Cerebral dysfunction type: The condition was relieved after admission, but repeated convulsions after 3 to 4 days, convulsions stopped within 2 days; neurological syndrome remained in the recovery period. This type of brain damage is lighter than fulminant hair. The mind changes or improves after more than 24 hours, and the muscle tension is normal or elevated. There are intermediate remission and recurrent seizures are clinical features, and there is no literature report. The time of recurrence may be related to the peak of cerebral edema 2 to 3 days after onset; it is related to regression after 1 week.
