Download Acute Renal Failure

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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:
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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
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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
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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.