ACUTE RENAL FAILURE
Acute Renal Failure is a sudden and almost complete loss of kidney function caused by failure Ge of the renal circulation/or by glomerular or tubular dysfunction.
It is frequently associated with an increased BUN and creatinine oliguria (< 500 ml urine/24 hrs.), hyperkalaemia and Na retention.
Causes
1. Prerenal causes result from conditions that renal blood flow albumin (hypovolemic, shock, haemorrhage, burns, impaired cardiac output diuretic therapy).
2. Postrenal causes arise from obstruction or disruption to urine flow anywhere along the urinary tract.
3 Intrarenal causes result from injury to renal tissue and are usually associated with intrarenal ischemia, toxins, immunologic processes, systemic and vascular disorders.
Clinical Phase of Acute Renal Failure
1. Onset: begins when the kidney is injured and lasts from hrs to days.
2 The period of oliguria, (oliguric - anuric phase)- (Urinary volume < 400-500 ml/24 Hrs.)
a Is accompanied by a rise in serum concentration of elements usually, excreted by kidneys (urea, creatinine, organic acids/uric acid, and the intracellular cations-K magnesium). Lasts approximately 10 days.
b. There can be a in renal function with increasing sodium retention yet the Patient is actually excreting 2 or more Liters of urine daily called nonoliguric or high output renal failure.
3 Period of diuresis (Diuretic phase): [the Pt experience a gradually increasing urinary output, which signals that glomerular filtration has started to recover] Begins when the 24 hour urine volume exceeds 500 ml And ends when the BUN and serum creatinine levels stop rising.
4 Period of recovery (Recovery phase): Usually lasts several months to 1 year, Signals the improvement of renal function, There is a permanent partial reduction in the glomerular filtration rate and the ability to concentrate urine.
Clinical Manifestations
1. Patient is critically ill and is lethargic with persistent/nausea, vomiting and diarrhoea Skin and mucous membranes are dry from dehydration. Breath may have the Odor of urine Drowsiness, headache, muscle, witching and convulsions, Urinary output- scanty may be bloody and has a low. electrolyte imbalance.
2. Specific gravity [(1.010/compared with 1.025 normally)] Rise in serum creatinine [with the rate of rise dependent on the degree of catabolism (breakdown of protein)] High serum potassium level [Protein catabolism results in the release of cellular k into the body fluids, causing serious k intoxication GFR is reduced has decreased ability to excrete K+]
3. Decrease in Na+ [from the GIT from diarrhoea and vomiting] Acute oliguria fall in blood Co2 combing power and blood ph leading to acidosis. Vit-D
4. Ser. Phosphate concentration and low ser. Calcium levels [in response to Ded Absorption of calcium from the intestine)
5. Anaemia [from blood loss due to uremic G1 lesions, reduced RBC life span and reduced erythropoietin production.
Diagnostic Evaluation
1. Urinalysis - reveals proteinuria, haematuria, casts.
2. Increased Serum Creatinine and BUN levels; [ratio is an high as 41:1]
3. Urine chemistry examination [to distinguish various forms to ARF) increased Na+
4. Renal ultrasonography for estimating the renal size and to exclude a treatable obstructive uropathy.
Medical Management
Preventive Measures
1. Identify Pts with preexisting renal disease.
2. Initiate adequate hydration before during and after any procedure requiring NPO status. Nil Per oral.
3. Avoid exposure to nephrotoxins. Be aware that the majority of drugs or their metabolites are excreted by the kidneys.
4. Avoid chronic analgesic abuse causes interstitial nephritis and papillary necrosis.
5. Prevent and treat shock with blood and fluid replacement. Prevent prolonged periods of hypo tension. Contral Venous Pressure.
6. Monitor urinary output and CVP hourly in critically ill pts to detect onset of renal failure at the earliest movement.
7. Schedule diagnostic studies requiring dehydration so there are 'rest days' especially in aged who may not have adequate renal reserve.
8. Pay special attention to draining wounds, burns, etc., which can lead to dehydration and sepsis and progressive renal damage.
9. Avoid infection give meticulous care to pts with indwelling catheters and I.V lines.
10. Take every precaution to ensure that the right. Person receives the right. Blood to avoid severe transfusion reaction which can precipitate renal complication.
Corrective A Supportive Measures
1. Early dialysis prevents complication of uraemia such as hyperkalaemia (k intoxication), pericarditis and seizures. (Dialysis correction of biochemical abnormalities; allows for liberation of fluid, protein & Na intakes; diminishes bleeding tendencies; and may help wound healing)
2. Monitor for hyperkalaemia - serum electrolyte Levels, ECG-peaked T waves and Patient evaluation.
Administration of exchange resins (sodium polystyrene sulfonate (Kayexalate)] orally or by retention enema.
Sorbitol induces H₂O loss in GIT given orally or as an enema with kayexalate. Watch for faecal impaction.
If a retention enema is given (the colon is the major site for K exchange), a
rectal catheter with a balloon may be prescribed to facilitate retention if necessary. The Pt should retain the resin 30-45 minutes to remove K.
- A patient with a high end rising levels of serum K requires immediate peritoneal dialysis, haemodialysis or hemofiltration.
- IV glucose and insulin or calcium gluconate- administer k+ for intoxication
- NaHCO3 Promotes an elevation of plasma pH, which causes K to move into the all & the result is lowering of K in the plasma.
- All ext. Sources of K. are eliminated are reduced.
3. Establish fluid balance daily today weight, serial measurements of CVP, sea & urine concentration, fluid losses BP & clinical status of the pt.
[fluid loss- parenteral & oral input, urine output, gastric drainage, stools, wound drainage& perspiration fluid loss through skin and lungs also considered].
4. Na+ losses are measured [(by evaluating serum urine Na levels)] are corrected
5. Adequate blood flow to the kidneys may be restored by IVF and medication. Mauston, furosemide, or ethacrynic acid prescribed to initiate a dieresis and prevent or minimize subsequent renal failure.
6. Lavande albumin may be given, if ARF is caused by hypovolemia 2º to hypo proteinuria
7. Treat shock and infection.
8. In severe acidosis, ABG is monitored and appropriate ventilatory measures are instituted if respiratory problems develop. Patient may require NaHCO3therapy or dialysis.
9. Phosphate binding agents (aluminium hydroxide) keeps phosphate from being absorbed into the bloodstream and helps preventing a continuous rise in serum phosphate levels.
10. Dietary proteins 1gm/kg during the oliguric phase (to minimize protein breakdown and to prevent accumulation of toxic end products.) Caloric requirement are met with high Cholesterol feedings (Since Cholesterol have a protein sparing effect in a high cholesterol diet. Protein is not used for meeting energy requirements but is "spared" for growth and tissue healing)) Restrict K to 40-50 mEq/day and Na-2gm/day. Restrict foods & fluids containing K & phosphorus (bananas, citrus fruits & juices, coffee). After the diuretic phase, a high-protein, high-caloric diet is given & the patient is encouraged to resume activities gradually since muscle weakness will be present from excessive catabolism.
11. Flood chemistry evaluation are made to determine the amounts of Na+, K+ & H₂O needed for replacement along with assessment for overhydration and underhydration.
Nursing Management
1. Measure and record 1/0 of all fluids, including wound drainage, NG tube output and diarrhoea.
2. Monitor for signs of infection. Remove ladder catheter as soon as possible; monitor for UTI; [use intensive pulmonary hygiene high incidence of lung edema and infection); carry out meticulous skin care; Adm. Antibiotics, care must be taken to adjust the dosage for renal impairment.
3. Weigh Patient daily. If necessary, measure abdominal girth daily. [Mark the skin with indelible ink so that measurements can be taken in the same place.]
4. Monitor for s/s of hypovolemia or hypervolemia, [ because regulating capacity of kidneys is inadequate]
5. Monitor serum and urine electrolyte concentration.
6. Adjust fluid intake to avoid volume overload and dehydration.
7. Measure BP regularly with patients sitting and standing position.
8. Inspect neck veins for engorgement and extremities, abdomen, sacrum and eyelids for edema.
9. Evaluate for s/s of hyperkalaemia and monitor serum k levels., Admi. Na HCO3 or glucose and insulin sulfonate (kayexalate) to provide more prolonged corrections of elevated K avoid food is K. Prepare for dialysis when rapid lowering of K. is needed and administer blood transfusions during dialysis to prevent hyperkalaemia from stored blood.
10. Monitor ABG for acid base balance, prepare for ventilator therapy [if severe acidosis is present and/or respiratory problems development]. administer NaHCO3 [for symptomatic acidosis) and prepare for dialysis if acidosis is uncontrolled.
11. Low protein diet may be supplemented with essential amino acid and vitamins. Protein will be Jed if the Pt is a dialysis to allow for the loss of amino acids occurring during dialysis.
12. Offer high CHO feedings because CHO have a greater protein sparring power of provide additional calories.
13. Restrict foods and fluids containing large amounts of Na, K, and phosphorus.
14. Examine all stools of emesis for gross and occult blood administer H2 receptor antagonist, adjust the dose for the degree of renal impairment.
15. Watch for and report mental status changes somnolence, lassitude, lethargy and fatigue progressing to irritability disorientation, twitching, seizures
16. Use seizure precautions padded side rails, airway and suction equipment at bedside.
17. Encourage and assist Patient to turn and move because drowsiness a lethargy may prevent activity.
18. Advise avoidance of any medication unless specifically prescribed.
Complication
1. Infection
2 Arrhythmia due to hyperkalaemia
3. Electrolyte (Na, K, Ca, Phosphorus) abnormalities.
4. G.I bleeding due to stress ulcers
5. Multiple organ systems failure.
