neonatal renal vein thrombosis
Introduction
Introduction to neonatal renal vein thrombosis Renal venous thrombosis (RVT) is renal vein thrombosis. Primary NRVT is mainly related to dehydration, increased blood viscosity and decreased renal blood flow. Blood thickening and increased blood viscosity reduce renal flow, renal oxygenation. Reduced, followed by renal edema, increased renal small blood vessel pressure, and ultimately lead to renal venous thrombosis. Its clinical manifestations lack specificity and are often masked by critical underlying diseases, so there is no exact data on morbidity and mortality. basic knowledge The proportion of illness: 0.001% Susceptible population: newborn Mode of infection: non-infectious Complications: Hypertension, jaundice, renal failure
Cause
Causes of neonatal renal vein thrombosis
(1) Causes of the disease
RVT is often caused by a variety of comprehensive causes.
Primary kidney disease (30%):
The early reports of RVT are caused by hypercoagulable state of the kidney during nephrotic syndrome, but neonatal renal diseases associated with NRVT are rare, and only renal nephrotic NRVT caused by congenital nephrotic syndrome or renal tumors. .
Increased blood viscosity (25%):
Such causes are most important in NRVT. In physiological conditions, there are more red blood cells in the peripheral blood of newborns. When feeding is insufficient, non-dominant water loss increases, and diuretics or contrast agents, birth injuries, asphyxia, hypoxia, ischemia, etc. are applied. The reason can make the blood thick and the blood viscosity increases exponentially.
Renal vascular pedicle involvement (15%):
Renal (main) venous circulation disorders caused by retroperitoneal abscess or umbilical vein cannulation, but such reports of extrarenal NRVT have been reported in recent years.
Reduced renal blood flow (10%):
Such as infection, shock, maternal pregnancy-induced hypertension syndrome or diabetes.
As early as the 1940s, Gross counted 47 cases of neonatal arterial embolism (including 4 cases of renal artery embolism) in the literature for more than 100 years. It is believed that infection, congenital heart disease, injury and post-natal umbilical arterial changes are possible diseases. The reason, since then, the continuous observation of NRAE has proposed different views on its possible pathogenesis, but so far, other causes are being explored in addition to umbilical artery cannulation.
(two) pathogenesis
Unlike the renal artery system, the renal vein system does not have any kind of segmental distribution. Only a series of arched veins that are consistent with each other connect the blood flow of the two poles of the kidney. There is no capillary network between the small arteries and the small veins. Interlobular and interlobular veins, which flow into the renal (main) vein through the renal medulla and renal hilum, the right renal vein only communicates with the ipsilateral ureteral vein, while the left renal vein can easily form a collateral circulation with the other four or five veins. .
The pathogenesis of NRVT depends on the rapidity of thrombus formation, location, size, completeness, and the balance between collateral circulation formation. Regardless of unilateral or bilateral lesions, the above conditions and primary underlying disease determine the disease. Clinical and imaging findings, even prognosis, increased blood thickening and increased blood viscosity, decreased renal flow, decreased renal oxygenation, followed by renal edema, increased renal vascular pressure, and ultimately renal venous thrombosis There are three types of processes for NRVT formation:
1. Acute complete embolization of acute edema of the kidney, the pressure in the renal capsule is increased sharply, the renal venous pressure can be increased by 20 times, the renal artery blood flow is reduced to 25% of the normal amount, or even completely stopped, the kidney is damaged and bleeding, The appearance of the kidney is blemish, and the kidney is swollen within 24 hours of the onset of the disease, reaching a peak at 7 days, and gradually shrinking after 2 months, which may become a residual atrophic kidney.
2. If the partial partial embolization is 80%-90%, the collateral circulation can occur in the other 24 hours after the onset of symptoms. The collateral anastomosis is optimal at 12 days to 1 month after the onset. Kidney size, imaging morphology and renal function can be restored 2 months after onset.
3. The degree of progressive embolization of the collateral anastomosis can be formed, and collateral anastomosis can be formed. In addition to albuminuria, renal function is often normal.
Prevention
Neonatal renal vein thrombosis prevention
Active prevention and treatment of gastrointestinal diseases, prevention and treatment of severe dehydration and reasonable feeding, prevention of asphyxia, hypoxia, birth injury, ischemia, etc., can increase blood viscosity, prevent infection, shock and maternal pregnancy-induced hypertension syndrome or Diabetes, etc., to reduce the cause of renal blood flow, prevention and treatment of neonatal erythrocytosis and high blood viscosity to prevent this disease.
Complication
Neonatal renal vein thrombosis Complications, hypertension, jaundice, renal failure
Often complicated by hypertension, acidosis, jaundice, renal failure; often combined with lung and limb embolism, spermatic vein or gastroesophageal varices.
Symptom
Neonatal renal vein thrombosis symptoms Common symptoms Abdominal pain Hematuria nausea Facial hemisphere Blue black nodules Dehydration Thrombosis Reduce bloating Venous thrombosis Jaundice Oliguria
Clinical classification
(1) Primary: The cause is concealed, hematuria, renal enlargement and thrombocytopenia. The extracellular fluid of neonates born to diabetic mothers can be reduced by 25%, so it is easy to cause congenital RVT.
(2) secondary: often caused by diseases other than the urinary system, such as congenital protein C and / or protein S deficiency, often fulminant purpura.
(3) Kidney-derived: rare in the neonatal period.
2. Clinical manifestations
The clinical manifestations of RVT in the neonatal period are lack of specificity and are often masked by the primary disease. Typical RVT has three main symptoms: abdominal pain, hematuria and renal enlargement, but abdominal pain is difficult to find in the neonatal period and is replaced by thrombocytopenia.
(1) Dehydration: Dehydration includes history, symptoms and signs of occult water loss.
(2) sudden hematuria and oliguria: sudden appearance of hematuria, oliguria or anuria, thrombocytopenia and hypertension, which are not directly related to the primary disease, 60% of children have 24 hours of gross hematuria, followed by persistence Microscopic hematuria, 36% of children have oliguria or no urine, proteinuria and acidosis are also more common, blood pressure suddenly rises and then rises sharply, high blood pressure can last for several days, months or more, can be accompanied by nausea , vomiting and bloating, fever, jaundice, systemic edema, lung and limb embolism, spermatic vein or gastroesophageal varices may also be seen.
(3) Kidney enlargement: 50% to 60% of children can reach the enlarged kidney. The size, thickness and tension of the kidney are different from those of the kidney under physiological conditions. The uneven feeling during fusion, the kidney hardness increases due to the increased tension in the renal capsule capsule, and the discomfort response is uncomfortable during palpation. The right lesion is more common on the left side. If both sides are involved, the size of each other must be Differences.
Examine
Neonatal renal vein thrombosis
Routine tests:
1. Blood examination is most important for thrombocytopenia and its dynamic observation, which helps to judge the activity or static of thrombosis.
2. Blood tests can be seen with positive tests for DIC.
3. Urine routine examination shows gross or microscopic hematuria.
Film degree exam:
Various imaging examinations of the kidney may be positive, but ultrasound is the most important.
1. X-ray plain film suspected and NRVT, especially congenital RVT, first take the abdominal plain film (posterior and lateral position) to estimate the size of the kidney and whether there is calcification in the kidney area, if the pregnant mother has diabetes, Neonatal calcification within 3 days after birth can be diagnosed as congenital RVT, and there are reports of intrauterine fetal RVT, but it has also been reported that renal calcification in very low birth weight is related to calcium supplementation or diuretics. It has nothing to do with congenital RVT.
2. Ultrasound examination is the first choice for detection methods and monitoring methods because it is painless, non-radioactive and non-invasive. It is divided into early, middle and late phases.
(1) Early: 7 days or so, but as early as 30 minutes after the onset of the disease, there is a positive observation. First, in the embolized renal lobular vein and inter-leaf vein, there are echo-enhanced fine stripes, which gradually spread and expand; the whole kidney is edema The echo is weakened, especially with a circular echo around the renal cone; the boundary between the renal cortex and the medulla is unclear; if the length of the kidney is increased by 13%, a 40% increase in volume can be determined as a kidney enlargement.
(2) Interim: On the 10th to 21st day of onset, echogenic waves are enhanced due to infiltration of renal parenchyma, hemorrhage or fibrosis; enhanced echogenic zone can be seen in the anechoic zone or adrenal gland of the kidney due to hemorrhage; renal cortex The boundary between the medulla and the medulla is clearer; the echogenicity of the dilated intrarenal vein and the perirenal vein can be seen.
(3) Late stage: late after 2 months, the kidney can return to normal; or see enhanced echo plaque shadow caused by renal calcification; or residual small kidney shadow, the surface is not smooth due to shrinkage, if The initial ultrasound examination is already the latter, and it is indistinguishable from congenital renal hypoplasia.
Doppler ultrasonography can confirm the presence or absence of blood flow in the blood vessels. Especially in the early stage, the renal venules can be found to have no blood flow during the diastolic phase. If the renal vein beats can be seen, the NRVT on the side can be excluded.
Diagnosis
Diagnosis and diagnosis of neonatal renal vein thrombosis
diagnosis
Critically ill newborns with history, symptoms and signs of dehydration (including occult water loss), and hematuria, renal enlargement, thrombocytopenia, and hypertension that are not directly related to the underlying disease, combined with ultrasound imaging, most NRVT can be diagnosed. If the mother has diabetes and the kidney has calcification within 3 days after birth, it can be diagnosed as congenital RVT. Currently, intrauterine fetal RVT has been reported. Intrarenal NRVT may only be seen during pathological examination. To renal hemorrhage and/or necrosis, it is not necessary to see renal vein thrombosis.
Differential diagnosis
The identification of sepsis and renal artery embolization should be emphasized. Both diseases may have consumptive coagulopathy and poor renal development. Positive blood culture often contributes to the diagnosis of these two diseases. Renal artery embolism is common in sepsis, umbilical artery. Intubation, patent ductus arteriosus, arrhythmia or trauma, less common than RVT, very few kidney involvement, kidney is not swollen, almost no gross hematuria, often with hypertension, peripheral blood and selective renal venous blood The increase in renin is mainly caused by antihypertensive and infection control.
