Prevention And Treatment Of Acute Renal Failure
Acute Renal Failure Patient
A General Overview
Prompt detection and treatment of prerenal factors causing hypotension and avoidance of potentially toxic drugs and toxins serve to prevent the development of acute renal failure. In conditions associated with hypovolemic shock, furosemide in doses of 1-2 mg/Kg body weight may be given to induce urine flow after correction of fluid volume by administration of intravenous fluids. Cases in which acute tubular necrosis has not set in, respond by increasing the urine output to 30-40 ml/hour over the next 2-3 hours. If the response is not satisfactory, it is safer to assume that the patient has developed acute tubular necrosis and institute suitable therapy.
Cardinal principles in the management of the oliguric phase are:
- To sustain life
- Prevent complications; and
- Give time for the natural recovery of the kidney
The “fluid intake output chart” and daily recording of body weight help in guiding fluid administration. In severe cases, monitoring of the central venous pressure is beneficial. Oliguric patients with fluid overload must have very strict restriction of fluids, with a view to achieve a daily weight loss of 0.2 to 0.5 kg. If there is no overhydration, 300-500 ml of fluid loss during the previous 24 hours. Cases of acute renal failure with normal urine output do not require rigorous restriction.
Sodium: Since sodium administration leads to fluid retention, sodium should be avoided totally during the anuric and severly oliguric phase. Measurement of serum sodium and urinary sodium will help in planning sodium administration in individual patients.
Potassium: Hyperkalemia and subsequent cardiac toxicity due to hyperkalemia are the most important life-threatening complications during the oliguric phase. Serial estimation of serum potassium and electrocardiographic changes of hyperkalemia include tall peaked T-waves, widening of QRS complex, prolongation of PR interval, disappearance of P-wave and cardiac arrest. The serum potassium levels may not correlate closely with the ECG changes. The ECG changes start appearing when the serum potassium level exceeds 5.5 meq/liter.
Hyperkalemia warrants total withdrawal of potassium from food and drinks. Fruits juices and stored blood are the common natural sources of potassium. The adverse cardiovascular effects of hyperkalemia are abolished by the intravenous administration of 10% calcium gluconate slowly. Administration of sodium bicarbonate corrects acidosis and shifts the potassium into the intracellular compartment. Calcium and sodium bicarbonate should be administered intravenously only with an interval of at least 10 minutes to avoid pharmacological imcompatibility. Administration of 25% glucose, 0 to 100 ml followed by 16 units of soluble insulin, helps in transferring the potassium from the extracellular to the intracellular compartment and thereby lower serum potassium. Potassium can be removed from the body by the use of potassium exchange resins (Keyexalate) or dialysis.
Dialysis And The Dialysis Machine
Treatment And Prognosis
Calories and Proteins
The diet should contain at least 2000 Cal with only 18-20g protein in 24 hours. High carbohydrate, high fat diet provides adequate calories. If the patient cannot take orally, it may be necessary to give 25 to 50% glucose through a canula into a major vein or inferior vena cava.
This can be corrected by intravenous administration of sodium bicarbonate which is indicated if the patient develops acidotic breathing or if the serum bicarbonate is less than 15 meq/liter.
In the majority of cases of acute tubular necrosis, the blood pressure is normal. Often the hypertension is related to fluid overload. Restriction of fluid and salt and diuretics bring down the blood pressure. Anti-hypertensive drugs are instituted if the above mentioned measures fail.
Blood transfusions are required for anemia only if packed cell volume falls below 20%.
This procedure is indicated if the condition persists with deterioration of the condition. If facilities are available, early dialysis should be instituted to prevent the development of azotemia and other complications. The results are much better with early or prophylactic dialysis.
Any drug which has presumably caused or aggravated acute renal failure must be discontinued. There is no role for prophylactic antibiotic treatment. The dosage of drugs used for treatment of active infection in acute renal failure to be modified suitably.
Liberal intake of fluids, sodium and potassium is allowed to patients during the diuretic phase. Dehydration, postural hypotension and weakness due to hypokalemia should be looked for daily. The protein intake may be increased to 40-60g/day. Normal diet can be resumed gradually.
In renal failure associated with serious infection, multiple injuries or when multiple factors are responsible, the mortality may range from 30-40%. In uncomplicated cases, the mortality is less than 10%. The mortality depends on the speed and efficiency of treatment.
© 2014 Funom Theophilus Makama