neonatal acute renal failure
Introduction
Introduction to neonatal acute renal failure Neonatal acute renal failure refers to neonatal low blood volume, shock, hypoxia, hypothermia, drug poisoning and other pathological conditions, the kidney is damaged in a short time, showing oliguria or anuria, body fluid disorder, acid Alkali dysregulation and the concentration of metabolites (urea, creatinine, etc.) that need to be excreted by the kidney in plasma are elevated. Acute renal failure is often a serious disease late complication, and it is one of the critical clinical syndromes of neonates. basic knowledge The proportion of illness: 0.004% Susceptible people: children Mode of infection: non-infectious Complications: hyperkalemia hyponatremia hypocalcemia metabolic acidosis high blood pressure heart failure pulmonary edema arrhythmia
Cause
Causes of neonatal acute renal failure
Prerenal factors (35%):
In the neonatal period, clinical factors that can reduce the amount of cardiac output or insufficient blood volume may cause renal perfusion low, leading to prerenal ARF, insufficient renal blood perfusion in neonates, most often within 48 hours after birth. A variety of pathological conditions, such as suffocation hypoxia, respiratory distress syndrome, heart failure, hypotension, severe dehydration, massive bleeding, sepsis, hypothermia, etc., positive pressure ventilation pressure can affect blood reflux to reduce cardiac output The use of high-dose vasodilators to lower blood pressure, or high-dose vasoconstrictors (such as norepinephrine) can cause renal vasospasm, renal renal perfusion is insufficient and pre-renal ARF occurs.
Renal factors (30%):
Caused by damage to the renal parenchyma, also known as true renal failure, the main causes are as follows:
(1) Kidney hypoxia: severe or prolonged suffocation may cause different degrees of kidney damage, mainly seen in perinatal hypoxia, in addition, neonatal frostbite and serious infection, etc., is also an important cause of neonatal renal parenchymal injury Mainly seen in children with hypothermia, hard swelling area >50%, hypoxemia and acidosis.
(2) renal ischemia: massive blood loss, renal artery (or renal arteriolar) thrombosis, embolism and stenosis, renal cortical or medullary necrosis, renal infarction, renal vein thrombosis (severe dehydration, DIC, poor circulation, diabetes mothers and babies ) Renal vascular disease can reduce renal blood flow and insufficient blood supply to the renal tubules.
(3) Kidney poisoning: including nephrotoxic antibiotics such as aminoglycoside antibiotics, polymyxin, amphotericin, etc.; easy to cause kidney damage drugs such as indomethacin, tolazoline and so on. Various kidney-induced toxic products such as hemoglobinuria, myosinuria, peroxideuria, uric acid nephropathy.
(4) Other renal diseases: congenital renal dysplasia such as no kidney development, bilateral renal cystic lesions, neonatal polycystic kidney disease, congenital syphilis, toxoplasmosis, congenital nephrotic syndrome and pyelonephritis.
Post-renal factors (35%):
Mainly caused by urinary tract obstruction ARF, seen in various congenital urinary tract malformations, such as posterior urethral valve, urethral diverticulum, foreskin atresia, urethral stricture, ureteral fistula, neurogenic bladder, etc., can also be seen in extra-renal tumor compression urethra or medical Source surgical intubation injury leads to urethral stricture.
Pathogenesis
The pathogenesis of neonatal ARF needs to be further explored, and the following changes are currently considered.
1. Decreased glomerular filtration rate: renal perfusion caused by various causes, vasogenic substances such as catecholamine, serotonin, histamine, angiotensin II and thromboxane, etc., release or activity, renal vasoconstriction, Increased resistance can cause glomerular filtration rate (GFR) to decrease and oliguria.
2. Leakage and reabsorption of renal tubules in the renal tubules: renal hypoperfusion, renal ischemia, hypoxia or nephrotoxic substances damage the renal tubular wall, tubular cell necrosis, shedding, basement membrane rupture, glomerular filtrate undergoes The damaged tubular cells and basement membrane infiltrate into the interstitial and leak back into the blood, and the damaged renal tubules are accompanied by reabsorption disorders, which promote oliguria or anuria and aggravate renal function damage.
3. Renal tissue cell metabolism disorder: In hypoxia, renal tissue oxidative phosphorylation disorder, ATP, ADP decreased, cell dysfunction, free radical production, lipid peroxide cell membrane damage, intracellular potassium decreased, sodium, Calcium influx, etc., the renal medullary rough ascending branch is more susceptible to hypoxia than the proximal curved tube.
4. Immune reaction: When a serious infection (caused by bacteria, viruses, etc.), the antigen-antibody complex of the immune response causes a series of reactions that can cause DIC, block renal capillary, increase vascular resistance, decrease GFR, and necrosis of the renal tubule.
Prevention
Neonatal acute renal failure prevention
ATN (acute tubular necrosis) still has a high mortality rate, so it is very important to take active preventive measures. It is necessary to give effective intervention in the transitional stage between pre-renal ARF and ATN to prevent structural damage of the kidney. Maintaining the balance of body fluid capacity, giving expansion treatment to correct the state of hypovolemia, and also dealing with cardiac insufficiency to maintain renal perfusion blood volume. Clinical evidence suggests that hydration therapy can prevent contrast agents, amphotericin B. , ATN caused by drugs such as cisplatin. Before chemotherapy in cancer patients, a certain water load should be given, and allopurinol and sodium bicarbonate should be used to prevent renal failure. The clinical capacity load state is sometimes difficult to judge. Therefore, it is necessary to increase vigilance for critically ill patients and establish an effective fluid replacement pathway. Invasive hemodynamic monitoring is needed. Infectious shock is also one of the main causes of ATN. Therefore, it is necessary to actively control infection, and at the same time take various measures to maintain blood pressure stability. Contrast agents should be used with caution for patients with impaired renal function. And other nephrotoxic drugs, in addition, low-dose dopamine, mannitol, loop diuretics, atrial natriuretic peptide, calcium antagonists, adenosine antagonists, oxygen free radical scavengers and growth factors and other drugs, in experimental research and not perfect The clinical observation suggests that it may be beneficial to the prevention of ATN, but there are many contradictory conclusions. Therefore, it is considered that the active treatment of the primary disease, maintaining the capacity balance (expanding if necessary) and stabilizing blood pressure are still the most important measures to prevent ATN.
Complication
Neonatal acute renal failure complications Complications hyperkalemia hyponatremia hypocalcemia metabolic acidosis hypertensive heart failure pulmonary edema arrhythmia
Often complicated by hyperkalemia, hyponatremia, hypocalcemia, hyperphosphatemia, metabolic acidosis, hypertension, heart failure, pulmonary edema and arrhythmia.
Symptom
Neonatal acute renal failure symptoms Common symptoms Anorexia tired expression Apathy Chest tightness Facial flushing Newborn proteinuria Drowsiness No nausea and nausea azotemia
1. General performance
(1) Non-specific symptoms: refusal to eat, vomiting, pale, and weak pulse.
(2) The main symptoms: oliguria or no urine, excessive fluid (occupation of edema, weight gain) can lead to high blood pressure, heart failure, pulmonary edema, cerebral edema and convulsions.
(3) Signs: edema, ascites, etc.
2. Clinical staging According to pathophysiological changes and conditions, it is divided into three phases: oliguria or anuria, polyuria and recovery.
(1) oliguria or anuria: the main performances include:
1 oliguria or no urine: neonatal urine volume <25ml / d or 1ml / (kg · h) for oliguria, urine output <15ml / d or 0.5ml / (kg · h) for anuria, neonatal ARF The duration of oliguric period varies, and the condition is critical for more than 3 days. In recent years, there have been reports of ARF in oliguric neonates, and the disease and prognosis are better than those with oliguria or no urine.
2 electrolyte disorder: neonatal ARF, often complicated by the following electrolyte disorders:
A. Hyperkalemia, blood potassium > 7mmol / L, due to reduced urinary potassium excretion, acidosis causes intracellular potassium transfer to the extracellular, may be associated with abnormal ECG: T wave towering, QRS widened, ST segment Shift and arrhythmia.
B. Hyponatremia, blood sodium <130mmol / L, mainly due to blood dilution or low sodium reabsorption.
C. High phosphorus, hypocalcemia, etc.
3 metabolic acidosis: due to decreased glomerular filtration function, hydrogen ion exchange and acid metabolite excretion disorders.
4 azotemia: ARF, protein metabolism products in the body from the renal excretion disorder and protein decomposition, blood non-protein nitrogen content increased, the emergence of azotemia.
(2) Polyuria: As the function of glomeruli and a part of renal tubules recovers, the amount of urine increases, and the general condition gradually improves. For example, the amount of urine increases rapidly, and patients may have dehydration, low sodium or hypokalemia. Severe observation of the condition and monitoring of blood biochemical changes should be observed.
(3) Recovery period: the general condition of the child improved, the urine volume gradually returned to normal, the uremia manifestation and blood biochemical changes gradually disappeared, the glomerular function recovered quickly, but the renal tubular function change lasted for a long time.
Examine
Examination of neonatal acute renal failure
1. Significant reduction in urine output: neonatal urine volume <25ml / d or 1ml / (kg · h) for oliguria, urine output <15ml / d or 0.5ml / (kg · h) for anuria, less urine At the same time, the relative density is low, and the urine routine is different due to the disease.
2. Nitrogenemia: serum creatinine (Scr) 88 ~ 142mol / L, blood urea nitrogen (BUN) 7.5 ~ 11mmol / L, or Scr increased by 44mol / L per day, BUN increased 3.57mmol / L.
3. Calculation of GFR: glomerular filtration rate (such as endogenous creatinine clearance) is often 30ml/(min·1.73m2) when conditions are available. The application of classical endogenous creatinine clearance rate is more complicated to evaluate GFR. The Schwartz formula can be used to calculate neonatal GFR and to evaluate neonatal ARF renal function status. The results are significantly positively correlated with the application of endogenous creatinine clearance values. Schwartz formula:
GFR (ml/min·1.73 m2) = 0.55 × L / Scr (L is the body length cm, and Scr is the plasma creatinine mg / dl).
4. Often accompanied by acidosis, water and electrolyte disorders: blood biochemical examination found that blood potassium, magnesium, phosphorus increased and sodium, calcium, chlorine decreased, carbon dioxide binding decreased.
5. Ultrasound examination of the kidney: It is a non-invasive examination method that can accurately describe the size, shape, water accumulation, calcification and bladder changes of the kidney. For patients with suspected renal vein thrombosis or progressive azotemia without cause, it should be done. This check.
6. Radionuclide kidney scan: understand renal blood perfusion, renal malformation, and a series of comparative judgments on glomerular filtration rate.
7. CT and magnetic resonance: help to determine post-renal obstruction.
Diagnosis
Diagnosis and diagnosis of neonatal acute renal failure
diagnosis
Diagnostic criteria for neonatal acute renal failure include the following:
1. Main performance: oliguria or anuria, no urination at 48h after birth or oliguria <1ml/(kg·h) or no urine <0.5ml/(kg·h) after birth, convulsions, refusal of milk, vomiting, etc.
2.Scr, BUN continued to increase: Scr88142mol/L, BUN7.511mmol/L, or Scr increased by 44mol/L every day, BUN increased 3.57mmol/L.
3. Blood biochemical changes: often accompanied by acidosis, water and electrolyte disorders.
Differential diagnosis
This disease can be caused by the kidney itself or extrarenal factors, should be identified at the time of diagnosis, pre-renal, renal ARF laboratory identification.
In the evaluation of neonatal ARF, early identification of neonatal prerenal, post-renal ARF, as far as possible to prevent their progression to renal ARF is extremely important.
1. Post-renal ARF: neonates with oliguria or anuria after birth, their maternal pregnancy history, maternal prenatal physical examination, fetal ultrasound and neonatal physical examination, the diagnosis of urinary tract obstructive disease is very Valuable, once suspected of obstruction, renal ureteral bladder ultrasound should be performed immediately.
2. Prerenal ARF
(1) Identification of prerenal and renal ARF: Compared with neonatal renal ARF, neonatal prerenal ARF urinary sodium excretion, lower sodium excretion score, urine/plasma osmotic pressure ratio, creatinine ratio are higher .
(2) Rehydration test: supplementing a certain amount of liquid is an effective method for clinically identifying prerenal and renal ARF, but it is disabled when the newborn suspects urinary tract obstruction or congestive heart failure. The method is 30 minutes. 20ml/kg isotonic liquid (usually normal saline) within 2h, if the urine volume is still less than 1ml/(kg·h) after 2h, and there is no insufficient circulating capacity, it may be renal ARF, which is widely used. The mannitol test for the diagnosis of prerenal ARF in children and adults may not be applied to newborns because of the sudden increase in serum osmotic pressure, which may cause intraventricular hemorrhage or white matter softening around the ventricles.
It should be noted that these indices that help identify prerenal and renal ARF have their limitations when applied to newborns. In neonates, urine/plasma creatinine ratio is evaluated in renal tubular reabsorption, compared to urine/ Plasma osmotic pressure ratio is more meaningful, which may be related to limited renal concentration regulation and low protein intake in neonates, especially premature infants.
