acute renal failure during pregnancy
Introduction
Introduction to acute renal failure during pregnancy Acute renal failure during pregnancy is a clinically very common disease. Acute acute injury of the renal parenchyma caused by any cause causes the nephron to lose its regulatory function, unable to maintain the balance of body fluids and electrolytes, and cannot excrete metabolites, resulting in hyperkalemia. Metabolic acidosis and uremic syndrome are collectively referred to as acute renal failure. In the early stage of acute renal failure during pregnancy, the clinical findings are often concealed by the symptoms of the primary disease, such as persistent shock caused by different causes, hemolysis reaction, symptoms of poisoning, etc., after several hours or 1 to 2 days, then enter Oliguria. Oliguria means less than 400ml of 24h urine or less than 17ml of urine per hour. Then 24h urine volume below 40ml, called no urine. Abnormally no urine is rare, complete renal dysfunction, acute renal cortical necrosis, glomerulonephritis and acute renal failure caused by malignant hypertension may appear completely auria. In a small number of patients with non-urinary acute renal failure, the amount of urine can be maintained at 800ml ~ 1000ml or more. The oliguria period is generally 7 to 14 days, the short is 2 to 3 days, and the elderly can be up to 2 months. Patients with oliguria over one month have a poor prognosis, and even if they are exempt from acute death, renal insufficiency is difficult to recover. basic knowledge The proportion of the disease: the incidence of this disease in pregnant women is about 0.03% - 0.04%, mostly in women with high blood pressure Susceptible population: pregnant women Mode of infection: non-infectious Complications: urinary tract infection
Cause
Causes of acute renal failure during pregnancy
(1) Causes of the disease
Factors leading to acute renal failure during pregnancy include hypovolemia caused by various causes, renal vasospasm and microvascular hemolysis, occasionally in the damage of poisons, and the main subjects are described later.
1. Insufficient blood volume A large amount of blood loss is seen in the placenta previa, early placenta stripping, stillbirth and postpartum hemorrhage; severe dehydration is seen in hyperemesis during pregnancy.
2. Renal vasospasm is a part of systemic vasospasm, which may be secondary to insufficient blood volume; endotoxin stimulation of toxic shock or specific manifestations of certain obstetric complications such as severe hypertensive disorder complicating pregnancy.
3. Microvascular hemolysis due to hemolysis, hemoglobinuria and cellulose emboli associated with glomerular capillaries cause damage to the kidney leading to acute renal failure, seen in acute fatty liver during pregnancy, HELLP syndrome.
4. Other occasional blood transfusions, amniotic fluid embolism, rarely due to obstructive acute renal failure caused by huge uterine compression of the ureter.
Insufficient blood volume and renal vasospasm are the most common factors leading to acute renal failure during pregnancy. Regardless of the initial factors, the two tend to exist at the same time in the progression of the disease, further aggravating the condition, and severe cases may be accompanied by diffuse blood vessels. Internal coagulation and microvascular hemolysis changes occur mostly in early exfoliation of severe placenta, stillbirth and severe hypertensive disorder complicating pregnancy.
(two) pathogenesis
The pathogenic factors of acute renal failure are different, and the pathophysiological processes are also different. The pathology and pathophysiology of acute renal failure caused by insufficient blood volume and renal vasospasm are described in detail in order to evaluate the condition. Timely discovery and treatment of various complications and improvement of prognosis.
1. The initial stage of renal failure
Due to insufficient blood volume, the body compensates for blood redistribution, first of all to ensure the supply of blood to the vital organs such as the heart and brain, and the renal blood flow is correspondingly reduced; other causes of renal vasospasm will also produce the same result, this period has not yet occurred. Histological changes, after timely treatment of renal function can still return to normal, it is also known as functional renal insufficiency.
2. The stage of renal parenchymal injury is also called acute renal failure oliguria, the pathogenic factors persist, and the renal blood flow is further reduced. In order to maintain a certain glomerular filtration rate, the occluded arterial compensatory contraction, and The arteries are the main source of nutrients in the renal tubules. Its sustained contraction will cause tubular ischemia and necrosis. This is a common pathological change, which is mild and can be repaired. When the renal blood flow is extremely reduced, 90% of the blood will be Does not flow through the glomerulus, and short circuit, resulting in renal cortical necrosis, which is an irreversible lesion, less common than the former, accounting for 12.7% to 29.5% of acute renal failure caused by obstetric causes, the consequences are serious, more There is residual chronic renal insufficiency, extensive renal cortical necrosis on both sides, and extremely high mortality, requiring long-term dialysis or kidney transplantation.
3. Recovery period of renal parenchymal injury
That is, acute renal failure during the polyuria period. After appropriate treatment, the renal tubular epithelial cells begin to repair soon after the onset of oliguria, but their function recovery is slower, mostly after 7-10 days or more. Beginning to recover, when the 24h urine volume increased by more than 400ml, it marked the beginning of this period.
4. Renal parenchyma healing period
Also known as the recovery period, with the recovery of renal function, the urine volume is gradually reduced, water, electrolyte imbalance and azotemia are corrected, and the constitution is also recovered, usually starting from the 2nd to 3rd month of the disease, requiring 3 to 6 In the month, there are also those who need more than one year. Some of these cases cannot be completely recovered due to severe kidney damage, leaving chronic renal insufficiency.
Prevention
Prevention of acute renal failure during pregnancy
1. Prevent the occurrence of primary disease
Strictly manage the indications, contraindications and methods of application of nephrotoxic drugs; strictly implement blood collection, blood matching and blood transfusion procedures, etc., to prevent acute renal failure caused by blood group incompatibility, which fundamentally prevent acute renal function The occurrence of exhaustion syndrome.
2. Actively rescue critically ill patients
Early control of diseases that induce acute renal failure, such as placental abruption, obstetric hemorrhagic shock, amniotic fluid embolism, and severe pregnancy-induced hypertension syndrome, are diseases that are highly susceptible to acute renal failure, so they should be actively treated when these diseases occur. Remove the primary lesion and terminate the pregnancy in time to prevent or reduce shock and disseminated intravascular coagulation, and control the induction of acute renal failure.
3. Quickly correct functional oliguria
Once the pathogenic factors lead to functional oliguria, measures should be taken quickly to restore normal, thus reducing the incidence of organic oliguria, the following measures can be taken:
(1) Actively supplement blood volume: If the clinical manifestations or the fluid replacement test proves that there is insufficient blood volume, appropriate measures should be taken to make up the foot. Before the blood is not matched, the balance solution or dextran can be quickly infused, and it is best to take a large amount of blood transfusion. Fresh blood within 6h, the blood transfusion rate is very important, it is best to make up within 2h, or at least 50%, if you can not get blood, you should lose as much as possible to the library blood within 5 days, and according to coagulation function test results and platelet count , as appropriate, with frozen fresh plasma and concentrated platelet products.
(2) Avoid using drugs that cause strong contraction of renal blood vessels. Trying to relieve renal vasospasm is the best measure to reduce acute renal failure and reduce mortality.
1 application of vasodilator drugs: papaverine 20 ~ 30mg intravenous injection; aminophylline 0.25g plus 10% glucose solution 20ml intravenous injection; atropine 0.5mg intravenous injection, the application of these drugs in amniotic fluid embolism can not only correct pulmonary hypertension, but also prevent Renal vasospasm, so that the renal tubules avoid necrotic damage.
220% mannitol or 25% sorbitol 125-250ml alone or with low molecular weight dextran 500ml fast intravenous infusion (but to prevent heart failure) to supplement blood volume, diuretic can improve renal blood circulation, reduce the incidence of tubular necrosis, Furosemide 100 ~ 200mg intravenously or in combination with mannitol can obtain similar or better results.
3 renal capsule closure or epidural anesthesia can also relieve renal vasospasm.
Complication
Complications of acute renal failure during pregnancy Complications, urinary tract infections
Can be complicated by urinary tract infection, effective blood volume deficiency, heart failure and so on.
Symptom
Acute renal failure symptoms during pregnancy Common symptoms Polyuria heart failure shock Hypertension Placental abruption Dehydration coma Nausea oliguria Apathy
Oliguria
In the early stage of the disease, the clinical findings are often concealed by the symptoms of the primary disease, such as persistent shock caused by different causes, hemolysis reaction, symptoms of poisoning, etc., after several hours or 1 to 2 days, then enter the oliguria period, Oliguria means 24h urine volume less than 400ml or hourly urine volume less than 17ml, and 24h urine volume below 40ml, called nouria, no urine is rare, complete urinary tract obstruction, acute renal cortical necrosis, kidney Acute renal failure caused by glomerulonephritis and malignant hypertension may result in complete anuria. In a small number of patients with non-urinary acute renal failure, the urine volume can be maintained at 800ml to 1000ml or more, and the oliguria period is generally 7 to 14 days. The short is 2 to 3 days, the elderly can reach 2 months, and the oliguria period is more than 1 month. The prognosis is poor. Even if it is free from acute death, renal insufficiency is difficult to recover.
In the oliguria period due to the retention of water, salt, and nitrogen metabolites, the following symptoms may occur:
(1) edema: due to oliguria, reduced water discharge, easy to cause water retention, but often accompanied by ascites and nausea, vomiting, so there is not necessarily edema at the beginning, most patients due to excessive infusion, tissue Edema, increased blood volume, elevated blood pressure, also known as water poisoning, and even heart failure, pulmonary edema and cerebral edema.
(2) Hypertension: In acute renal failure, renal ischemia and increased renin secretion are the main causes of hypertension, and the fluid load during oliguria is excessive, which is also aggravated by the fact that blood pressure is mostly 140-200. /90 ~ 110mmHg (18.7 ~ 26.7 / 12 ~ 14.7kPa), about 1 / 3 patients with normal blood pressure.
(3) Heart failure: On the basis of myocardial damage, if you do not pay attention to water and salt control during treatment, you may develop heart failure, chest tightness, shortness of breath, sitting breathing, coughing, foamy or pink, heart enlargement, There is a galloping horse, and the lungs are covered with wet squeaks or wheezing sounds. If you are not actively rescued, you may die.
(4) Electrolyte disorder: due to oliguria, acidosis, high blood potassium, high blood magnesium, high blood phosphorus, low sodium, low chlorine and hypocalcemia, high blood potassium clinical manifestations of limb numbness, reflex disappearance, heart rate Abnormalities, even ventricular fibrillation, cardiac arrest and ECG changes, low sodium, low calcium, acidosis can aggravate potassium poisoning, hyponatremia can show fatigue, muscle spasm, blood pressure drop, hypotonic coma, etc., high blood Magnesium symptoms are similar to hyperkalemia.
(5) Metabolic acidosis: due to renal dysfunction, uric acidation is weakened or disappeared, and various acidic metabolites and lactic acid accumulated by protein metabolism may cause metabolic acidosis, and patients may be weak and sleepy. Even coma.
(6) Nitrogenemia: In acute renal failure, due to the substantial increase in blood non-protein nitrogen and other metabolites, uremia symptoms, loss of appetite, nausea, vomiting, bloating, diarrhea and nervous system symptoms.
(7) Infection: acute renal failure makes the body's resistance weakened, immune function is low, in addition to the primary disease such as trauma, surgical infection, many treatments such as catheterization, injection, dialysis, etc. increase the chance of infection, patients often Combined with lungs, urinary tract, oral infections, sepsis is also common.
(8) Others: such as anemia and bleeding tendency, hemoglobin decreased, pale complexion and nail bed, subcutaneous ecchymosis, hematoma at the injection site, gastrointestinal bleeding.
2. Polyuria
(1) Urine: After timely and effective treatment of acute renal failure, after several days to 2 weeks, the renal lesions begin to repair. When the urine volume increases from oliguria or anuria to more than 400 ml, the renal function begins. One manifestation of recovery, the urine volume gradually increases or rapidly multiplies, and the daily urine output exceeds normal, up to 5000-7000ml/d. The polyuria stage indicates an improvement in renal blood flow and glomerular filtration rate, but the renal tubular weight The absorption function has not recovered. At this time, the patient's self-conscious symptoms are rapidly improved. After 2 weeks of urine, the diluting function of the renal tubules begins to recover. During this period, the urine specific gravity can be as low as 1.002. After 1 to 2 months, the dilution function can be restored. Normal, after 2 to 3 months of the disease, the kidney concentration function begins to recover. At this time, the specific gravity of the urine can be gradually increased to 1.015 to 1.018. It usually takes 1 year to reach 1.025 or more. If the urine specific gravity cannot be increased, it is fixed at Around 1.010, indicating a poor prognosis.
(2) Electrolyte disorder: When the patient's daily urine output exceeds 1000ml, a large amount of sodium salt is lost, and a large amount of sodium salt is lost, hyponatremia occurs, the patient shows weight loss, weakness, facial paralysis, and blood pressure. Inferior, because the function of the renal tubules is not yet perfect, plus a large amount of urination, a large amount of potassium ions are excreted with the urine. If potassium is not timely, hypokalemia can occur, and the patient shows weakness in muscle weakness, paralysis, difficulty breathing, bloating, heart Expanded, severe cases can be sudden death due to ventricular fibrillation and other A-S syndrome, hypocalcemia can occur during the polyuria, and increase the stress of neuromuscular.
(3) azotemia: in the polyuria period due to the structure and function of the renal tubule is not perfect, the clearance rate of the kidney is still very poor, so the retention of nitrogen metabolites is obvious, within 2 to 4 days of the beginning of the polyuria period The blood urea nitrogen can continue to rise and reach a peak, causing the clinical manifestations to not improve, sometimes worsening, and the heavy ones die. Later, with the increase of urine volume, the concentration of nitrogen metabolites gradually decreases, but the speed is slower. The patient's general condition began to improve rapidly, the spirit improved, and the appetite increased gradually. After a few weeks, the nitrogen metabolites gradually decreased to normal levels.
In the polyuria period, there may be low fever, which is prone to infection. Therefore, we should continue to observe the condition and strengthen supervision.
3. Recovery period
After the patient has oliguria and secondary urine, the tissue is destroyed and consumed. Therefore, it often shows weakness and weakness during the recovery period. Anemia, weight loss, muscle atrophy, and sometimes symptoms of peripheral neuropathy often take 3 to 6 months. It will not be fully recovered even after one year.
Examine
Examination of acute renal failure during pregnancy
Oliguria
(1) urine:
1 urine volume: urine is acidic, 24h urine volume is less than 400ml, observe the urine volume per hour, is the best way to find acute renal failure early, so place the catheter early, calculate the urine volume; if the patient cooperates, urinating once a hour to avoid the infection of the indwelling catheter.
2 Urine specific gravity: the early specific gravity can be normal or increased, and the subsequent decrease is fixed at about 1.012; if the urine specific gravity is higher than 1.020, it means dehydration.
3 urine formation: functional oliguria, usually only transparent or fine-grained tube type, acute tubular necrosis, a large number of epithelial cell casts, denatured cell casts, coarse-grained casts and a large number of renal tubular epithelial cells Hematuria, hemoglobinuria, pigmented casts, necrotic epithelial cell casts, etc.
4 urinary sodium concentration: in the oliguria period, renal tubular damage, so that the recovery of sodium salt decreased, so the increase in urinary sodium, the concentration is often 30 ~ 60mmol / L.
(2) blood routine: the total number of white blood cells can reach 20 × 109 / L, neutrophils can reach 80% ~ 95%; the degree of anemia depends on blood loss, hemolysis and nitrogen retention, hematocrit often drops 20% to 25%, when there is diffuse intravascular coagulation, the platelet count is reduced.
(3) Blood chemistry: Urea nitrogen, creatinine, serum potassium concentration increased, serum sodium, chlorine, calcium, carbon dioxide binding decreased, in acute tubular necrosis, renal tubular absorption of water decreased, urine urea and blood urea The ratio is often below 15 and the ratio of urinary creatinine to serum creatinine drops below 20.
(4) Urinary-plasma osmotic pressure ratio: This ratio reflects the ability of the renal tubule to concentrate and dilute. When the renal tubule is damaged, the ratio is often below 1.15 due to its poor concentration function.
(5) Diuretic test: In the case of blood volume supplementation, the patient still has no obvious increase in urine volume, and a diuretic test can be used to identify it. First, intravenous injection of 20% mannitol 100-125ml, urine volume per hour does not exceed 40ml, indicating kidney Functional failure; if mannitol is ineffective, switch to furosemide 40 ~ 60mg intravenously, urine per hour more than 40ml, still indicates good kidney function.
2. Polyuria
(1) 24h urine volume increased to more than 400ml, urine volume can reach 2500 ~ 3000ml after a few days; urine specific gravity is still low, starting at about 1.010, can be as low as 1.002; urine abnormalities gradually disappeared, urine The tube type subsides faster, white blood cells often increase, and it begins to retreat in a few weeks, which may be a mild infection of the urinary tract.
(2) As the condition improves, the blood biochemical abnormality can return to normal in a short period of time. The initial stage of urea nitrogen can continue to rise, and then gradually decline; when the urine volume is particularly high, hypokalemia and hyponatremia may occur.
(3) Anemia gradually recovers.
3. Recovery period
The 24h urine volume recovered to about 1500ml; the improvement of renal function was determined by kidney disease. After long-term follow-up, some patients' kidney function could be completely restored to normal, but some patients had chronic renal insufficiency symptoms.
1.B Ultrasound examination should be performed without any urine to exclude obstruction caused by stones.
2. Electrocardiogram helps to diagnose hyperkalemia and understanding the heart condition.
3. Central venous pressure measurement accurately understand the cyclic load.
4. In the differential diagnosis
Broken vaginal angiography, kidney map, kidney scan, renal angiography, etc. can often be used to identify urinary tract obstruction, prerenal oliguria or renal vascular disease.
Diagnosis
Diagnosis and diagnosis of acute renal failure during pregnancy
diagnosis
Detailed medical history, such as placenta previa, placental abruption, postpartum hemorrhage, severe pregnancy-induced hypertension, blood group incompatibility, etc. The pathogenesis and treatment of acute renal failure, etc., for acute renal failure without obvious causes, must be carefully reviewed History, such as shock, blood loss, kidney poisoning, etc.; persistent long-standing symptoms such as vomiting, anemia and activity intolerance, central nervous system depression, bone pain, polyuria, polydipsia, etc.; and previous blood urea nitrogen and Creatinine concentrations provide evidence of renal insufficiency.
The diagnosis of acute renal failure should pay attention to the history, symptoms, physical examination, comprehensive analysis of laboratory tests, major bleeding, shock or infection history, still oliguria after shock and recovery of blood volume, urine volume after diuretic application still does not increase, Clinically diagnosed as acute renal failure.
Differential diagnosis
Lack of urine
Need to identify is due to insufficient blood volume, or renal parenchymal damage has occurred, the former showed significant thirst, pulse rate, normal or decreased blood pressure, small pulse compression, urine concentration, central venous pressure <0.59kPa (6cmH2O), under close observation After the liquid is replenished, the amount of urine increases. When the blood volume is corrected, the urine volume does not increase, indicating that the renal blood vessels have persistent sputum or renal parenchymal damage. If the urine volume is increased after using a diuretic, the former is likely to be large, otherwise it indicates that it has entered. Acute renal failure oliguria.
2. Renal tubular necrosis and renal cortical necrosis
The two reflect the severity of the disease and directly affect the prognosis. When acute renal failure occurs in the early stage of pregnancy, age > 30 years old, oliguria or anuria lasts for > 10 days, the latter is highly likely, selective renal angiography In the arterial phase, the branches of the arcuate artery or interlobular artery disappeared, the renal capsule blood vessels were coarse, and the renal phase showed a shallow fossa defect in the cortical area. The transparent area of the renal cortex of CT scan was helpful for the early diagnosis of renal cortical necrosis.
