Renal failure symptoms

Renal failure symptoms

Typical symptoms: abdominal pain in the lower abdomen, neonatal proteinuria, localized renal necrosis, head dizzy, chest tightness, indifferent expression, oliguria.

Related symptoms: abdominal pain in men, neonatal proteinuria, localized renal necrosis, head, chest, chest, chest, chest, facial expression

1 the clinical manifestations of oliguria or oliguria phase were nausea, vomiting, headache, dizziness, irritability, fatigue, lethargy, and coma. Due to the accumulation of water and sodium in the urine, the patient may have high blood pressure, pulmonary edema and heart failure. When the metabolites of protein can not be excreted by the kidney, the accumulation of nitrogenous substances in the body. When accompanied by infection, injury, fever, protein catabolism accelerated, blood urea nitrogen, creatinine increased rapidly, that is, the formation of uremia. The main features of this period are:

(1) decrease in urine volume: the volume of urine is reduced or gradually reduced, the amount of urine per day is less than 400ml, which is known as oliguria, less than 100ml is called non urine. Patients with ATN had no complete urine, and the prognosis was poor in patients with persistent urinary tract obstruction. As a result of the cause of disease and the severity of the disease, the duration of oliguria is not consistent, generally 1 to 3 weeks, but a few cases of oliguria for more than 3 months. It is generally considered that the duration of renal toxicity is short, and the duration of ischemia is longer. If the urine is less than 12 weeks, the diagnosis of ATN should be reconsidered. In the period of oliguria, attention should be paid to fluid retention, congestive heart failure, hyperkalemia, hypertension and complications.

Non oliguria type ATN, refers to the patient in the progressive period of nitrogen in the urine volume of more than 500ml, or even 1000 ~ 2000ml. The incidence of non oliguria has increased in recent years, up to 30% ~ 60%. The reason for this type of people and improve the understanding of renal toxicity, antibiotics are widely used and diuretics such as furosemide and mannitol on early application. There are 3 reasons for the decrease in urine volume:

The degree of impairment of renal units was different, the renal blood flow and glomerular filtration function of small renal units were present, but the renal tubular reabsorption function was significantly impaired.

The degree of renal tubular dysfunction was the same in all renal units, but the proportion of renal tubular reabsorption dysfunction was much lower than that of glomerular filtration function.

The ability to reduce the formation of renal medulla deep hyperosmolar state, resulting in the loop of Henle filtrate water reabsorption decreased. The common causes of non oliguria are the long-term use of nephrotoxic drugs, abdominal surgery and open heart surgery. Generally, non oliguric although less urine type light condition, shorter hospital stay, lower percentage of dialysis, upper gastrointestinal bleeding and other complications, but the incidence of hyperkalemia and oliguria caused a similar mortality nonoliguric rate is still as high as 26%. Therefore, in the treatment can not ignore any link.

(2) of azotemia due to reduced glomerular filtration rate caused by little or no urine, resulting in discharge of nitrogen and other waste reduction, plasma creatinine and urea nitrogen increased, the increased speed and protein decomposition state. In the absence of complications and correct treatment of cases, daily blood urea nitrogen increased slowly, about 3.6mmol/L (10mg/dl), increased plasma creatinine concentration was 44.2 ~ 88.4 mol/L (0.5 ~ 1.0mg/dl), but in the high decomposition state, such as with extensive tissue trauma and sepsis, every day can increase the blood urea nitrogen 7.1mmol/L (20mg/dl) or above, every 176.8 mol/L increased serum creatinine (2mg/dl) or above. The factors that can promote the decomposition of protein are insufficient heat supply, muscle necrosis, hematoma, gastrointestinal bleeding, fever, adrenal cortical hormone and so on.

(3) disturbance of water, electrolyte and acid-base balance:

Too much water in the water: strict control, the amount of fluid intake or excessive water, such as sweating, vomiting, estimation of wound infiltration amount is not accurate and the liquid volume calculation in water supplement is ignored. It is easy to produce too much water, which is characterized by diluted hyponatremia, soft tissue edema, weight gain, hypertension, acute heart failure and brain edema.

The hyperkalemia: normal intake of 90% potassium excretion from the kidney, ATN in oliguria stage because the urine excretion of potassium reduced, if at the same time in the presence of high resolution, such as crush muscle necrosis, hematoma and infection, inadequate intake of heat caused by the body protein decomposition, release potassium, acidosis intracellular potassium transfer to the extracellular, sometimes serious hyperkalemia occurred in a few hours in. If the patient is not timely diagnosis, more potassium intake of food or drink, penicillin drip of large dose of intravenous (per 1 million U penicillin potassium 1.6mmol); bleeding blood (input a large inventory of stock 10 days per liter of blood potassium containing up to 22mmol); also cause or aggravate hyperkalemia. In general, the etiology of ATN in the absence of complications of blood potassium per day rose less than 0.5mmol/L. Hyperkalemia can no characteristic clinical manifestations, or nausea, vomiting, numbness of the limbs paresthesia, slow heart rate, severe neurological symptoms, such as fear, irritability, consciousness, until the late sinoventricular or atrioventricular block, sinus arrest, intraventricular block or ventricular fibrillation. ECG changes of hyperkalemia can precede the clinical manifestation of hyperkalemia. Therefore, it is very important to monitor the effect of hyperkalemia on myocardium. The general blood potassium concentration in the 6mmol/L, ECG showed tall and narrow base of T wave, P wave disappeared with blood potassium increased, QRS increased, S-T can not be identified, the final fusion with T wave, followed by the emergence of serious arrhythmia, and ventricular fibrillation. The effect of high potassium on myocardial toxicity in vivo is affected by the concentration of the sodium and calcium and acid-base balance, while there are hyponatremia, hypocalcemia or acidosis, hyperkalemia ECG performance significantly, and easily induced arrhythmia. It is worth mentioning that there are some inconsistencies between serum potassium concentration and ECG performance. Hyperkalemia is one of the most common causes of death in patients with oliguria. However, severe muscular tissue necrosis often occurs with persistent hyperkalemia. In order to control the hyperkalemia, the necrotic tissue should be removed completely.

The metabolic acidosis: normal human daily fixed acid metabolites is 50 ~ 100mmol, 20% of them combined with bicarbonate excreted by the kidney, 80%. Acute renal failure, because of acid metabolites in urine decreased, renal tubular acid secretion ability and preservation of sodium bicarbonate decreased, resulting in daily plasma bicarbonate concentration decreased in different degrees; more faster decrease in high decomposition state. Most of the endogenous acid is from the decomposition of protein, a small part from sugar and fat oxidation. Phosphoric acid and other organic anions are released and accumulated in the body fluid, resulting in increased anion gap in this patient, the continuous case of oliguria if metabolic acidosis can not be fully corrected, fast decomposition of the body muscles. In addition, acidosis can reduce ventricular fibrillation threshold, the occurrence of ectopic rhythm. Hyperkalemia, severe acidosis and low calcium, hyponatremia is a serious illness in acute renal failure, dialysis patients have been relatively rare, but in some cases still need dialysis drugs to correct metabolic acidosis.

The hypocalcemia and hyperphosphatemia: ATN low calcium and hyperphosphatemia in chronic renal failure is outstanding, but there were reports of oliguria 2 days of hypocalcemia. Because at the same time often accompanied by acidosis, so that the extracellular calcium ions increased, it does not occur in the common clinical manifestations of low calcium. Due to hypocalcemia hyperphosphatemia caused by normal intake of phosphate from 60% to 80% after the urine. In the period of ATN, there is a slight increase in serum phosphorus, but if there is a significant metabolic acidosis, hyperphosphatemia is also more prominent, but significantly increased. After the correction of acidosis, serum phosphorus can be decreased to some extent. If the cases of continuous intravenous nutrition therapy should be paid attention to, the occurrence of hyperphosphatemia should be noticed.

Hyponatremia and low blood pressure: both exist at the same time. Can cause hyponatremia due to water caused by excessive dilutional hyponatremia, due to burns or vomiting and diarrhea from skin or gastrointestinal loss caused by, or non oliguric patients of high dose furosemide has reaction lose sodium hyponatremia. Severe hyponatremia can lead to blood osmotic concentration decreased, resulting in water penetration into cells, cell edema, acute cerebral edema symptoms, clinical manifestations of fatigue, weakness, lethargy or disturbance of consciousness, disorientation, and hypotonic coma. Hyponatremia is common in vomiting

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