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1 NUR409 Acute Renal Failure -Occurs in 2-5% of patients admitted to a general medical-surgical unit and in up to 23% of critical care patients. -Usually strikes individuals who are already critically ill. -Associated with 50% mortality rate. General A&P review (do not consider these reminders as a comprehensive review!) -Kidneys receive ~ 20-25% of the cardiac output. Arterial blood travels through the renal artery and reaches the glomerulus via the afferent arteriole. Blood leaves the glomerulus through the efferent arteriole. Blood eventually leaves via the renal vein. -The glomerulus is a cluster of tiny blood vessels that filter blood. -As blood flows through each glomerulus, water, electrolytes and waste products are filtered out of the blood, across the glomerular membrane and into Bowman’s capsule where a filtrate is formed. -At normal filtration rates of 125 ml/min, the kidneys produce 180L of filtrate each day. As the filtrate passes through the various components of the nephron’s tubules, 99% of the filtrate is reabsorbed into the bloodstream. Eventually, the remaining filtrate (only 1% of the original 180L/day) is excreted as urine. This provides an average urine output of 1 to 2L/day. -The kidneys also help maintain acid-base balance. Acute Renal Failure -sudden deterioration of renal function resulting in retention of nitrogenous waste products (azotemia). It is usually accompanied by oliguria (U.O.<400ml/24 hrs). -ARF is caused by 3 categories of conditions: prerenal, postrenal and intrinsic (intrarenal or parenchymal). The category is determined by the precipitating factor. PRERENAL: interference with renal perfusion. Examples: 3 rd spacing fluid, hemorrhage, hypotension, renal artery vasoconstriction. We intervene by correcting the condition that is causing hypoperfusion of the kidney. INTRARENAL: disease or injury of the actual kidney. Examples: nephrotoxic medications or overdose; glomerulonephritis; acute tubular necrosis POSTRENAL: caused by obstruction of the urinary tract. ATN may occur after prolonged ischemia, exposure to nephrotoxic substances or a combination of factors. Some patients have ATN after only several minutes of hypotension or hypovolemia whereas others can tolerate hours of renal ischemia without experiencing any problems. -Damage occurs to the glomerular basement membrane and tubular epithelium (especially @ the proximal tubule.) -People who develop ATN usually have complete recovery. Course of ATN: 2 1. Initiation phase: period of time between the occurrence of the precipitating event to the beginning of the change in urine output. Spans several hours to 2 days during which the normal renal processes begin to deteriorate. 2. Maintenance phase: intrinsic renal damage is well established. Urine output is at its lowest point during this phase. Lasts 8 to 14 days but may last as long as 1 to 11 months. Longer a patient remains in this stage, the slower the recovery and the greater the chance of permanent renal damage. Complications during this phase: uremia, hyperkalemia, infection. 3. Recovery phase: Renal tissue recovers and repairs itself. Gradual increase in urine output and an improvement in lab values. Some patients may have a large diuresis during this phase caused by salt and water accumulation in extracellular spaces; osmotic diuresis resulting from retained waste products; diuretics given to speed up salt and water excretion. Recovery can take from 4 to 6 months. NURSING CARE CONCERNS R/T ARF: 1. Obtain subjective data: symptoms, PMH, exposure to nephrotoxins; risk factors, dye studies, diagnostic tests, medication history. 2. Physical assessment: assess for signs of uremia. Hydration status? Vital signs 3. Laboratory values: assessment of the urine is extremely valuable in the evaluation of ARF. Best measure of renal function is urinary creatinine clearance. (creatinine is a metabolic byproduct of creatine and phosphocreatine in the muscles. Since muscle mass does not rapidly alter, levels of creatinine produced by the body remains pretty constant. This means that creatinine levels tend to reflect changes in renal function.) Procedure for creatinine clearance: a. patient empties his/her bladder. Record exact time. Throw out the urine specimen. b. All urine for the next 24 hours is saved. c. Exactly 24 hours after the start of the procedure, patient voids again and the specimen is saved. d. Serum creatinine is assessed at the end of the 24 hours e. All the urine that was saved is sent to the lab for testing. f. Normal creatinine clearance is about 125 ml/min. 4. If a 24-hour creatinine clearance is not done, the next best measure of renal function is the serum creatinine level followed by the serum BUN level. BUN is the least accurate measure of kidney functioning since it can be influenced by many factors. 5. May also perform random urine electrolyte samplings. When urinary sodium is being retained, indicates that the kidneys are attempting to conserve sodium and water. On the other hand, if urinary sodium levels are high, may mean that the diseased tubules are having difficulty reabsorbing electrolytes. 6. VOLUME OF URINE IS NOT A GOOD INDICATOR OF RENAL FUNCTION. 7. Measure I & O and daily weights. 8. Watch for the impact of ARF on other body systems. a. cardiovascular: fluid volume overload 3 b. hematologic: increased susceptibility to infection secondary to invasive tests, decreased ability to fight infection, anemia c. respiratory: uremia impairs normal immune response of the lungs and suppresses the cough reflex. Sputum becomes thick and tenacious. Fluid volume overload if oliguric. d. Gastrointestinal: anorexia, nausea, vomiting, stomatitis, bleeding (a slow ooze rather than hemorrhage) that increases the BUN. e. Neuromuscular: cerebral edema, changes in mental status, seizures, tremors. f. Integumentary: yellowness of skin due to retention and excretion of urochrome pigment through the skin (this is what gives urine its yellow color). Duller yellow than jaundice and does not affect the sclerae of the eyes. MEDICAL/NURSING INTERVENTIONS 1. if possible, relieve underlying cause 2. diuretics 3. prevent infection (do not automatically use an indwelling foley with people that have ARF). Use strict aseptic technique with all IV lines. 4. Drug therapy including dopamine (1 to 3 mcg/kg/min) 5. Remember that drug therapy in people with ARF is particularly troublesome since about 2/3 of all drugs or their metabolites are eliminated from the body by the kidney. Usually have to adjust dosages. Monitor peak and trough levels. Remember that drugs that are water-soluble are removed by dialysis. 6. Dietary management: Average metabolic rates in ARF are about 20% higher than normal causing increased catabolism. 7. Fluid imbalance generally managed by dietary restriction of salt and water and administration of diuretics and low-dose Dopamine. 8. Electrolyte imbalances: Electrolyte imbalance Etiology Clinical signs/symptoms hyperkalemia Decreased excretion of ECG changes; tall T waves; potassium muscle weakness; abdominal cramps and diarrhea Hyponatremia Fluid retention & oliguria Nausea and vomiting; headache (d/t cerebral edema), fatigue, weakness, seizures Hypocalcemia Decreased kidney excretion Parasthesias, tetany, of Phosphorus (remember seizures, +Chvostek’s sign, when phosphorus goes up, +Trousseau’s sign calcium goes down) Hyperphosphatemia Decreased excretion of Same signs as hypocalcemia phosphorus Hypermagnesemia Decreased excretion of Lethargy, coma, hypotension, magnesium flaccid muscles, prolonged PR interval and QT interval, bradycardia, heart block TREATMENT OF HYPERKALEMIA: 1. calcium gluconate 10 ml of a 10% solution given IV over 5 minutes 4 2. glucose (50 ml of 50% dextrose) given IV w/regular insulin, 10U given IV 3. sodium bicarbonate 50 to 100 mEq/l given IV 4. Kayexalate (sodium polystyrene sulfonate) 15 to 30 gm given every 3 to 4 hours with a 20% sorbital solution given by mouth or as a retention enema. TREATMENT OF HYPONATREMIA: 1. fluid restriction (free water) TREATMENT OF HYPERPHOSPHATEMIA: 1. Calcium supplements. 2. restrict dietary intake of phosphorus 3. administration of phosphate-binding agents (aluminum hydroxide gels and calcium carbonate). Protein-rich and calcium rich foods are also high in phosphorus so restrict the intake of these food types. We used to administer aluminum hydroxide gels as a standard of care (eg. Amphogel, Alternagel). Discovered possible link between elevated aluminum levels and Alzheimer’s Disease—in addition to other concerns. Now, standard of care is Calcium supplementation. So, when you have a patient receiving Oyster Shell or Oscal, do NOT assume that the drug is to treat osteoporosis. More likely, if the patient has renal failure, the issue is phosphate control.