The basic elements of diagnosis
- The sudden emergence of oliguria. The amount of urine 20-200 ml / day.
- Proteinuria and hematuria. Izostenurija with a specific gravity of urine from 1010-1016.
- Anorexy, nauzea and vomiting, lethargy, high blood pressure. Signs of uremia.
- Progressive increase in serum urea, creatinine, potassium, phosphate, sulfate. The reduction of sodium, calcium and CO3 concentrations.
- Spontaneous recovery in a few days.
General Considerations
Under acute renal failure podrazumcvamo sudden cessation of renal function that occurs after various insults in an otherwise healthy kidneys. The following causes can lead to acute renal failure: (1) toxic agents, eg. carbon tetrachloride, mercurv bichlorid, arsenic, diethylene glycol, sulfonamides and mushroom poisoning, (2) traumatic shock after a serious injury, surgical shock, myocardial infarction, renal ischemia, resulting in surgical intervention on the abdominal aorta, (3) destruction of tissue caused by karst injuries, burns, intravascular hemolysis, (4) Infectious diseases eg. leptospirosa, hemorrhagic fever, septicemia gram-negative bacteria (septic shock), (5) severe dehydration and electrolyte disturbances, (6) pregnancy complications eg.: bilateral cortical necrosis.
The re-establishment of renal function can be expected, but even the most appropriate aggressive therapy on appearing, the mortality rate is high. Renal tubular necrosis is a characteristic finding. In some cases, after exposure to specific toxins, primarily damaged proximal tubule. In both kidneys, occurs uniformly disintegration of renal tubule cells, their deskvamaciaj and collecting their remains in the lumen of the tubule. In other cases, in addition to the destruction of tubular cells, there is damage to the basement membrane and end. In case of violation of hemolysis or limestone, may be cylindrical or myoglobin heme, but they differ from us Tali cylinder destruction of tubular cells.Speckled distribution of damage is consistent with changes in the blood that cause ischemic necrosis.In bilateral cortical necrosis, ishemičnj infarcts are deployed in both kidneys.
Clinical findings
The cardinal sign of the development of acute renal failure is a decrease in urine output after injury, surgery, blood transfusion, incompatible, or other causes listed above. Diurcza within 24 hours may be reduced to only 20-30 ml per day, and this reduction was not so hard, so patients 400-500 ml of urine excreted per day. After a few days to 6 weeks, slowly increasing the diuresis. Anorexia, and lethargy nauzea are common symptoms. Other symptoms and signs related to the causative agent or consequences. The course of the disease can be divided into diuiretičnu and oliguric phase.
A. Oliguric phase: during the oliguric phase of urine is very reduced. Urine contains proteins, erythrocytes, granular cylinders. The specific gravity of urine is usually 1010-1016. Speed increases of end products of metabolism in the body fluids, depends on protein catabolism. In the case of trauma or fever, serum urea, creatinine, potassium, phosphate, sulfate, and organic acids are rapidly increasing. Because of dilution and intracellular movement, the serum sodium concentration drops to 120-130 mEq / Iitar, with a corresponding decrease in serum chloride. If organic acids and phosphates accumulate in the serum bicarbonate concentration in serum decreases. Normochromic anemia is common. With prolonged oliguria, there are signs of uremia: nauzea, vomiting, diarrhea, irritability, neuromuscular, convulsions, somnolence and coma. Often develop hypertension, which can be accompanied with retinopathy, left ventricular failure and eneefalopatijom. During this phase of the disease, curing by significantly modifies the clinical picture. Hiperhiđracija causes intoxication with water, followed by convulsions, edema and sometimes very serious complications - pulmonary edema.Giving large amounts of salt can lead to edema and Brake heart failure. Errors related to potassium intake, or if you do not use agents for the removal of potassium at the right time, can lead to intoxication with potassium. High level of extracellular potassium causes neuromuscular depression that progresses to paralysis: disturbances in cardiac conduction pathways leading to the formation of arrhythmias. Death can result from respiratory muscle paralysis or cardiac arrest. While the increase in serum potassium ECG shows peaked Ttalas initially, and then expand QRSkompleksa Ptalasa loss.The severe degree of hyperkalemia appears biphasic ventricular complex occurs at the end of a cardiac arrest or ventricular fibrillation. If appropriate aggressive therapy on appearing potassium intoxication is almost always reversible and death is rare.
B. Diuretic phase: after a few days to 6 weeks after the occurrence of oliguria begins diuretic phase, indicating that the nephrons recovered from taoke in which the excretion of urine possible. Diuresis usually increases gradually from a few milliliters to 100 ml per day until 300-500 ml after which the rate of increase is usually much higher. Rarely had the receiver increases the excretion of urine during the first day or the day after uspostavijanja diuresis. Diuresis can lead to the deterioration nefronske function and loss of water and electrolytes, but this is rare and is running a deficit of water, sodium and potassium occurs only in rare cases. More often, diuresis is the release of excess extracellular fluid that accumulated during the oliguric phase of hyperhydration during aggressive therapy on appearing due to unusual or metabolic water production. Diuresis usually occurs when the total nefronska function is insufficient to secrete urea, potassium and phosphate mind. The concentration of these substances in the serum that can continue to grow for a few days after the elimination of one liter of urine a day. Renal function was slowly returning to normal, and biochemical blood tests become normal.
Differential Diagnosis
Because acute glomerulonephritis, urethral obstruction due to edema at the junction ureterovezikalnom uretcralne after catheterization or due to neoplasm, bilateral renal artery occlusion due to embolism or aneurysm disekantne and rarely rupture the bladder, may be accompanied by symptoms and signs that are indistinguishable from those with tubular necrosis, they need to be off the appropriate diagnostic procedures if they are suspected on the basis of history and physical examination. Sometimes difficult condition can cause severe dehydration Oliguria. Rapid infusion of 500-1000 ml of 0.45% sodium chloride will increase the volume of blood to the point where it will improve the glomerular filtration rate, which will lead to the establishment of diuresis.
Treatment
A. Specific treatment: removal of the causes which led to the oliguria important thing is for the treatment of acute renal failure.
First Shock - to eliminate renal ischemia is necessary to take serious measures to restore blood pressure to normal levels. Note: If you have already occurred tubular necrosis fluid intake must be very limited. If needed vazopresorni drugs they must be given only in the permitted amounts of liquids.
Second Transfusion reaction: see section 10
3rd Obstruction uretena: Occasionally, ureteral catheterization and cystoscopy.
4th Heavy metal poisoning: Dimercaprol (BAL) may be useful in arsenic or mercury poisoning, although at the time of occurrence of renal lesions its effect may be too late.
B. General measures: slodeća scheme of conservative treatment often is sufficient and adequate for uncomplicated cases. If oliguria lasts longer than a week or if the patient has suffered severe trauma, or if a strong "catabolic" state because of infections and toxins is indicated dialysis. Hemodialysis is effective and peritoneal dialysis may be of benefit. Indications for dialysis are precursors to hyperkalemia, severe hyperhydration or elevation of serum electrolytes, or the inability to maintain a relatively stable state with increase of oliguria.
First Oliguric phase. - The purpose of therapy is to maintain a normal body fluid volume and electrolyte concentrations, reduction of tissue catabolism to a minimum and prevent infection during treatment.
a. Bed rest: patients isolated to protect the mtrahospitalnih infekoija.
b. Liquids: limit fluid intake to basal needs of 400 ml per day for the average adult. Additional fluids may be given in order to compensate losses due to unusual vomiting, diarrhea, sweating, etc.. During the metabolism of fats, carbohydrates and proteins created by burning water, and tissue catabolism produces intracellular water. These water sources must be included in the calculation of the water balance, and for them there is only a small amount of water that is allowed as input. (See section E).
c. Diet: In order to limit the sources of nitrogen, potassium, phosphorus and sulfate, prohibit entry protein. Glucose, 10-200 gm per day, given in order to prevent ketosis and reduce protein catabolism.Although fat can be given to the patient in the form of butter or emulsions for oral or intravenous use, it is usually better that the patient realizes caloric needs from their own fat depots. Fluid and glucose can be given orally or intravenously. When given intravcnski 20-50% glucose, 400 ml of fluid should be given continuously for 24 hours through an intravenous catheter that is inserted into a large vein in order to reduce the risk of thrombosis. Should be given vitamin B complex and vitamin C.
d. Compensation electrolyte: prcdhodne offset losses. In other words, the electrolyte therapy is not necessary, unless there is a clear loss for example. vomiting, diarrhea and so on. Note: Potassium must not be given if there is no deficit in his case this gives very carefully.
email. Observation: daily recording of fluid intake and losses is essential. Bladder catheterization is usually required in order to exact measurement of diuresis. It is necessary whenever it is possible to follow the course of the day the body weight of the patients. Because the patient consumes its own tissue, you should lose about 0.5 pounds per day. If the patient does not lose weight he has received too much fluid. It is important to measure serum electrolytes (particularly potassium) and creatinine several times a day. ECG may help in assessing the level of potassium in the serum.
f. Infection: It takes a rigorous treatment of infection with appropriate antibiotics but it should be noted that drugs can be excreted through the kidneys. Isolation of patients is very useful protective measure.
g. Congestive heart failure: see section 8
h. Anemia: hematocrit less than 30% is an indication for transfusion careful it is best washed erythrocytes.
and. Potassium intoxication
j. Uremia: artificial kidney and peritoneal dialysis are effective but require supervision in well-equipped hospitals. With the proper equipment, dialysis proved evils of great value if the use of "prophylactic" when it is obvious that it is. Conservative treatment is insufficient to prevent acidosis, uremia progression and clinical deterioration.
k. Convulsions and encephalopathy: given paraldehid, rectally. Barbiturates should be limited to pentobarbitalNa amobarbitalNa them to be metabolized by the liver. Chlorpromazine and promazin are also useful.
Second Diuretic phase: unless there is a clear deficit of water and electrolytes, should not be given fluids and electrolytes (for the purpose of forcing diuresis); collection of excess water and electrolytes will be extracted. Liquid and dietary intake can be liberalized if urine output progressively increased until it reaches the normal daily intake. Protein restriction should be continued until no urea and creatinine begin to shrink. Infection is a risk in the diuretic phase. Sometimes diuresis may be accompanied by sodium retention, hypernatremia and hiperhloremijom, followed by confusion, neuromuscular irritability and coma. In this case they must be given in sufficient quantity of water and glucose, to correct hipernatremiju. Is often necessary to measure electrolytes, urea and creatinine levels.
Forecast
If there are no serious complications in the form of trauma or infection, skillful flow often overcome the oliguric phase and spontaneous healing. Death may occur due to water intoxication, Brake heart failure, acute pulmonary edema, potassium intoxication and encephalopathy. Consequence of curing the disease is damage to the small degree of renal function.
Of the authors:
Dr. Henry Brainerd, professor of medicine
Dr. Marcus A. Krupp, Professor of Medicine
Dr. Milton J. Chatton, Professor of Medicine
Dr. Sheldon Margen, professor of medicine
- The sudden emergence of oliguria. The amount of urine 20-200 ml / day.
- Proteinuria and hematuria. Izostenurija with a specific gravity of urine from 1010-1016.
- Anorexy, nauzea and vomiting, lethargy, high blood pressure. Signs of uremia.
- Progressive increase in serum urea, creatinine, potassium, phosphate, sulfate. The reduction of sodium, calcium and CO3 concentrations.
- Spontaneous recovery in a few days.
General Considerations
Under acute renal failure podrazumcvamo sudden cessation of renal function that occurs after various insults in an otherwise healthy kidneys. The following causes can lead to acute renal failure: (1) toxic agents, eg. carbon tetrachloride, mercurv bichlorid, arsenic, diethylene glycol, sulfonamides and mushroom poisoning, (2) traumatic shock after a serious injury, surgical shock, myocardial infarction, renal ischemia, resulting in surgical intervention on the abdominal aorta, (3) destruction of tissue caused by karst injuries, burns, intravascular hemolysis, (4) Infectious diseases eg. leptospirosa, hemorrhagic fever, septicemia gram-negative bacteria (septic shock), (5) severe dehydration and electrolyte disturbances, (6) pregnancy complications eg.: bilateral cortical necrosis.
The re-establishment of renal function can be expected, but even the most appropriate aggressive therapy on appearing, the mortality rate is high. Renal tubular necrosis is a characteristic finding. In some cases, after exposure to specific toxins, primarily damaged proximal tubule. In both kidneys, occurs uniformly disintegration of renal tubule cells, their deskvamaciaj and collecting their remains in the lumen of the tubule. In other cases, in addition to the destruction of tubular cells, there is damage to the basement membrane and end. In case of violation of hemolysis or limestone, may be cylindrical or myoglobin heme, but they differ from us Tali cylinder destruction of tubular cells.Speckled distribution of damage is consistent with changes in the blood that cause ischemic necrosis.In bilateral cortical necrosis, ishemičnj infarcts are deployed in both kidneys.
Clinical findings
The cardinal sign of the development of acute renal failure is a decrease in urine output after injury, surgery, blood transfusion, incompatible, or other causes listed above. Diurcza within 24 hours may be reduced to only 20-30 ml per day, and this reduction was not so hard, so patients 400-500 ml of urine excreted per day. After a few days to 6 weeks, slowly increasing the diuresis. Anorexia, and lethargy nauzea are common symptoms. Other symptoms and signs related to the causative agent or consequences. The course of the disease can be divided into diuiretičnu and oliguric phase.
A. Oliguric phase: during the oliguric phase of urine is very reduced. Urine contains proteins, erythrocytes, granular cylinders. The specific gravity of urine is usually 1010-1016. Speed increases of end products of metabolism in the body fluids, depends on protein catabolism. In the case of trauma or fever, serum urea, creatinine, potassium, phosphate, sulfate, and organic acids are rapidly increasing. Because of dilution and intracellular movement, the serum sodium concentration drops to 120-130 mEq / Iitar, with a corresponding decrease in serum chloride. If organic acids and phosphates accumulate in the serum bicarbonate concentration in serum decreases. Normochromic anemia is common. With prolonged oliguria, there are signs of uremia: nauzea, vomiting, diarrhea, irritability, neuromuscular, convulsions, somnolence and coma. Often develop hypertension, which can be accompanied with retinopathy, left ventricular failure and eneefalopatijom. During this phase of the disease, curing by significantly modifies the clinical picture. Hiperhiđracija causes intoxication with water, followed by convulsions, edema and sometimes very serious complications - pulmonary edema.Giving large amounts of salt can lead to edema and Brake heart failure. Errors related to potassium intake, or if you do not use agents for the removal of potassium at the right time, can lead to intoxication with potassium. High level of extracellular potassium causes neuromuscular depression that progresses to paralysis: disturbances in cardiac conduction pathways leading to the formation of arrhythmias. Death can result from respiratory muscle paralysis or cardiac arrest. While the increase in serum potassium ECG shows peaked Ttalas initially, and then expand QRSkompleksa Ptalasa loss.The severe degree of hyperkalemia appears biphasic ventricular complex occurs at the end of a cardiac arrest or ventricular fibrillation. If appropriate aggressive therapy on appearing potassium intoxication is almost always reversible and death is rare.
B. Diuretic phase: after a few days to 6 weeks after the occurrence of oliguria begins diuretic phase, indicating that the nephrons recovered from taoke in which the excretion of urine possible. Diuresis usually increases gradually from a few milliliters to 100 ml per day until 300-500 ml after which the rate of increase is usually much higher. Rarely had the receiver increases the excretion of urine during the first day or the day after uspostavijanja diuresis. Diuresis can lead to the deterioration nefronske function and loss of water and electrolytes, but this is rare and is running a deficit of water, sodium and potassium occurs only in rare cases. More often, diuresis is the release of excess extracellular fluid that accumulated during the oliguric phase of hyperhydration during aggressive therapy on appearing due to unusual or metabolic water production. Diuresis usually occurs when the total nefronska function is insufficient to secrete urea, potassium and phosphate mind. The concentration of these substances in the serum that can continue to grow for a few days after the elimination of one liter of urine a day. Renal function was slowly returning to normal, and biochemical blood tests become normal.
Differential Diagnosis
Because acute glomerulonephritis, urethral obstruction due to edema at the junction ureterovezikalnom uretcralne after catheterization or due to neoplasm, bilateral renal artery occlusion due to embolism or aneurysm disekantne and rarely rupture the bladder, may be accompanied by symptoms and signs that are indistinguishable from those with tubular necrosis, they need to be off the appropriate diagnostic procedures if they are suspected on the basis of history and physical examination. Sometimes difficult condition can cause severe dehydration Oliguria. Rapid infusion of 500-1000 ml of 0.45% sodium chloride will increase the volume of blood to the point where it will improve the glomerular filtration rate, which will lead to the establishment of diuresis.
Treatment
A. Specific treatment: removal of the causes which led to the oliguria important thing is for the treatment of acute renal failure.
First Shock - to eliminate renal ischemia is necessary to take serious measures to restore blood pressure to normal levels. Note: If you have already occurred tubular necrosis fluid intake must be very limited. If needed vazopresorni drugs they must be given only in the permitted amounts of liquids.
Second Transfusion reaction: see section 10
3rd Obstruction uretena: Occasionally, ureteral catheterization and cystoscopy.
4th Heavy metal poisoning: Dimercaprol (BAL) may be useful in arsenic or mercury poisoning, although at the time of occurrence of renal lesions its effect may be too late.
B. General measures: slodeća scheme of conservative treatment often is sufficient and adequate for uncomplicated cases. If oliguria lasts longer than a week or if the patient has suffered severe trauma, or if a strong "catabolic" state because of infections and toxins is indicated dialysis. Hemodialysis is effective and peritoneal dialysis may be of benefit. Indications for dialysis are precursors to hyperkalemia, severe hyperhydration or elevation of serum electrolytes, or the inability to maintain a relatively stable state with increase of oliguria.
First Oliguric phase. - The purpose of therapy is to maintain a normal body fluid volume and electrolyte concentrations, reduction of tissue catabolism to a minimum and prevent infection during treatment.
a. Bed rest: patients isolated to protect the mtrahospitalnih infekoija.
b. Liquids: limit fluid intake to basal needs of 400 ml per day for the average adult. Additional fluids may be given in order to compensate losses due to unusual vomiting, diarrhea, sweating, etc.. During the metabolism of fats, carbohydrates and proteins created by burning water, and tissue catabolism produces intracellular water. These water sources must be included in the calculation of the water balance, and for them there is only a small amount of water that is allowed as input. (See section E).
c. Diet: In order to limit the sources of nitrogen, potassium, phosphorus and sulfate, prohibit entry protein. Glucose, 10-200 gm per day, given in order to prevent ketosis and reduce protein catabolism.Although fat can be given to the patient in the form of butter or emulsions for oral or intravenous use, it is usually better that the patient realizes caloric needs from their own fat depots. Fluid and glucose can be given orally or intravenously. When given intravcnski 20-50% glucose, 400 ml of fluid should be given continuously for 24 hours through an intravenous catheter that is inserted into a large vein in order to reduce the risk of thrombosis. Should be given vitamin B complex and vitamin C.
d. Compensation electrolyte: prcdhodne offset losses. In other words, the electrolyte therapy is not necessary, unless there is a clear loss for example. vomiting, diarrhea and so on. Note: Potassium must not be given if there is no deficit in his case this gives very carefully.
email. Observation: daily recording of fluid intake and losses is essential. Bladder catheterization is usually required in order to exact measurement of diuresis. It is necessary whenever it is possible to follow the course of the day the body weight of the patients. Because the patient consumes its own tissue, you should lose about 0.5 pounds per day. If the patient does not lose weight he has received too much fluid. It is important to measure serum electrolytes (particularly potassium) and creatinine several times a day. ECG may help in assessing the level of potassium in the serum.
f. Infection: It takes a rigorous treatment of infection with appropriate antibiotics but it should be noted that drugs can be excreted through the kidneys. Isolation of patients is very useful protective measure.
g. Congestive heart failure: see section 8
h. Anemia: hematocrit less than 30% is an indication for transfusion careful it is best washed erythrocytes.
and. Potassium intoxication
j. Uremia: artificial kidney and peritoneal dialysis are effective but require supervision in well-equipped hospitals. With the proper equipment, dialysis proved evils of great value if the use of "prophylactic" when it is obvious that it is. Conservative treatment is insufficient to prevent acidosis, uremia progression and clinical deterioration.
k. Convulsions and encephalopathy: given paraldehid, rectally. Barbiturates should be limited to pentobarbitalNa amobarbitalNa them to be metabolized by the liver. Chlorpromazine and promazin are also useful.
Second Diuretic phase: unless there is a clear deficit of water and electrolytes, should not be given fluids and electrolytes (for the purpose of forcing diuresis); collection of excess water and electrolytes will be extracted. Liquid and dietary intake can be liberalized if urine output progressively increased until it reaches the normal daily intake. Protein restriction should be continued until no urea and creatinine begin to shrink. Infection is a risk in the diuretic phase. Sometimes diuresis may be accompanied by sodium retention, hypernatremia and hiperhloremijom, followed by confusion, neuromuscular irritability and coma. In this case they must be given in sufficient quantity of water and glucose, to correct hipernatremiju. Is often necessary to measure electrolytes, urea and creatinine levels.
Forecast
If there are no serious complications in the form of trauma or infection, skillful flow often overcome the oliguric phase and spontaneous healing. Death may occur due to water intoxication, Brake heart failure, acute pulmonary edema, potassium intoxication and encephalopathy. Consequence of curing the disease is damage to the small degree of renal function.
Of the authors:
Dr. Henry Brainerd, professor of medicine
Dr. Marcus A. Krupp, Professor of Medicine
Dr. Milton J. Chatton, Professor of Medicine
Dr. Sheldon Margen, professor of medicine
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