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Acute renal failure and early oliguria or anuria of the clin

2017-02-06 14:32

(A) the early: When the body after the onset of the shock and other causes, the lack of blood volume, blood pressure, renal vascular contraction occurs, renal blood flow reduction, glomerular filtration rate is also reduced, so that decreased urine volume, to increase the body reaction The antidiuretic hormone, aldosterone and adrenocorticotropic hormone secretion, so that further reduction of urine output, increased the proportion of urinary sodium decreased. This issue to the lack of blood volume and renal vasospasm-based, clinically only the primary disease symptoms and oliguria. This period is important to prevent the development of acute renal failure, if properly treated in a timely manner, that can avoid the development stage of organic renal failure.

(B) of oliguria or anuria: the persistence of pathogenic factors can cause renal damage, mainly renal tubular epithelial cell degeneration and necrosis, so as to enter oliguria or anuria. Where the 24-hour urine volume less than 400 ml were called oliguria, less than 100 ml were called anuria. The main clinical manifestations are:

1. Water excretion disorder

(1) oliguria or anuria: the mechanism of oliguria ① renal blood flow reduction, decreased glomerular filtration rate to reduce the formation of urine. ② renal interstitial edema, increased pressure, and further affect renal blood flow, leading to oliguria. ③ tubular epithelial basement membrane rupture, luminal and renal interstitial, urine flow reversibly to the renal interstitium, back to the venous system. Pigment tubular obstruction of renal tubular obstruction of urine. Reduced urine output during oliguria can occur suddenly or gradually. Oliguria generally lasts 7 to 14 days. The shorter the oliguria, the better prognosis. Non-oliguric acute renal failure in patients with urine volume is not reduced. Current urine acidic reaction, the proportion of fixed at 1.010 from top to bottom, generally below 1.014. Hemolytic type or extrusion of acute renal failure patients may have hemoglobinuria or myoglobinuria. Urine examination may have a protein, microscopic examination of red blood cells, granules or red blood cells and other tube. Urinary sodium content increased, urea and creatinine concentration decreased.

(2) water intoxication: in the kidney to reduce urination and metabolic exuberant and produce too much water in the case, such as excessive intake of liquid and sodium, can produce water intoxication. This is a serious complication of oliguria, the clinical manifestations of systemic soft tissue edema, acute pulmonary edema and cerebral edema. Pulmonary edema at the beginning of only the bottom of the lungs and respiratory tone reduction, severe lung full of vesicular breath sounds, and breathing difficulties, lips and other purple. Headache, vomiting, confusion and convulsions. Water poisoning on the one hand can be due to excessive body water retention, increasing the burden on the heart, causing heart failure; the other hand can lead to electrolyte imbalance, thus endangering the lives of patients. Therefore, water intoxication is one of the major causes of death in acute renal failure.

2. electrolyte imbalance

(1) The main manifestations of hyperkalemia circulatory system signs, such as slow heartbeat, arrhythmia, blood pressure, severe heart failure can be caused by poly stop. Followed by the performance of irritability, demeanor trance, unresponsive, hand, foot and paresthesia, muscle pain, numbness and other limbs. ECG changes are often not obvious before the clinical symptoms have been shown. Such as T wave towering, P wave disappeared, QRS widened, and even ventricular fibrillation, cardiac arrest and so on.

Hyperkalemia symptoms and the emergence of patients with serum sodium and calcium concentration. Serum sodium and calcium concentration of normal symptoms are not necessarily obvious, and serum sodium and calcium concentration decreased when prone to symptoms. If there are acidosis, the symptoms of hyperkalemia are more prone to.

(2) hyponatremia: acute renal failure when hyponatremia is more dilute hyponatremia. The reason is that extracellular fluid increases, sodium is diluted, sodium ions used to neutralize acidic substances with the urine and from the extracellular into the cell and potassium ion replacement. Only in the event of acute renal failure before vomiting, diarrhea, large area burns, etc., it may occur true of sodium deficiency hyponatremia. Generally mild hyponatremia often asymptomatic, or only manifested as burnout, eye socket subsidence, dizziness, apathy and so on. Severe cerebral edema can occur, leading to hypotonic coma.

(3) hyperphosphatemia: When renal failure when the phosphate excretion is affected, the formation of hyperphosphatemia. It does not produce symptoms, but can affect the concentration of calcium in the blood, making it more declining.

(4) hypocalcemia: due to phosphorus excretion from the kidneys and obstacles to the intestinal excretion, and calcium combined with non-absorption of phosphate and the formation of hypocalcemia.

(5) hypermagnesemia: Under normal circumstances, magnesium is mainly discharged by the kidneys, so renal failure can produce hypermagnesemia. Normal blood magnesium 1.5 to 2.5 meq / liter, once the blood magnesium higher than 6 milliq / l will appear when the symptoms, such as deep tendon reflexes, tachycardia, a variety of heart block, blood pressure, muscle paralysis Such as severe drowsiness and coma.

3. Metabolic acidosis: acute renal failure due to acid retention and consumption of excessive alkali storage, coupled with renal tubular hydrogen production capacity of ammonia, resulting in sodium and alkaline phosphate can not be recovered and retained, leading to metabolism Sex to Poisoning. This acidosis is often progressive, and difficult to completely correct, the clinical manifestations of weakness, lethargy, and even coma, heart weakness, blood pressure, and can aggravate hyperkalemia.

4. Azotemia: acute renal failure in vivo protein metabolites can not be excreted from the kidneys, coupled with infection, trauma, can not eat, etc., the body catabolism strong protein, causing a significant increase in blood non-protein nitrogen content , Clinically appear azotemia and urinary poisoning symptoms. Mild were no significant clinical symptoms. Moderate nausea and vomiting, and then there abdominal distension, diarrhea and other gastrointestinal symptoms. Severe drowsiness, coma and even death.

5. Hypertension: acute renal failure patients, about 2/3 of patients with varying degrees of hypertension, mainly due to renal ischemia and produce too much pressure material.

6. Heart failure: heart failure is one of the major complications of oliguria, often occurs in pulmonary edema and high blood pressure should be strictly observed.

7. Bleeding tendency: acute renal failure due to platelet defects, increased capillary fragility, thrombin generation was inhibited, may have significant bleeding tendency, mainly for epistaxis, subcutaneous ecchymosis, oral gingival and digestive tract Bleeding.

8. Anemia: Almost all cases have progressive anemia. The causes of anemia, on the one hand is due to trauma, bleeding, hemolysis caused by excessive loss and destruction of red blood cells; the other is due to toxic substances uremic inhibition of bone marrow red blood cell formation.

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