Acute renal failure

25 Acute renal failure




Overview/pathophysiology


Acute renal failure (ARF) is a sudden loss of renal function as a result of reduced blood flow or glomerular injury, which may or may not be accompanied by oliguria. The kidneys lose their ability to maintain biochemical homeostasis, causing retention of metabolic wastes and dramatic alterations in fluid, electrolyte, and acid-base balance. Although alteration in renal function usually is reversible, ARF may be associated with a mortality rate of 40%-80%. Mortality varies greatly with the cause of ARF, patient’s age, and comorbid conditions.


Causes of ARF are classified according to development as prerenal, intrinsic, and postrenal. A decrease in renal function secondary to decreased renal perfusion but without renal parenchymal damage is called prerenal failure. Causes of prerenal failure include fluid volume deficit, shock, and decreased cardiac function. If hypoperfusion has not been prolonged, restoration of renal perfusion will restore normal renal function. A reduction in urine output because of mechanical obstruction to urine flow is called postrenal failure. Conditions causing postrenal failure include neurogenic bladder, tumors, and urethral strictures. Early detection of prerenal and postrenal failure is essential because, if prolonged, they can lead to parenchymal damage. Restoration of renal function in cases of postrenal failure is directly related to removal of the obstruction.


The most common cause of intrinsic or intrarenal failure, or renal failure that develops secondary to renal parenchymal damage, is acute tubular necrosis (ATN). Although typically associated with prolonged ischemia (prerenal failure) or exposure to nephrotoxins (aminoglycoside antibiotics, heavy metals, radiographic contrast media), ATN also can occur after transfusion reactions, septic abortions, or crushing injuries. Additional medications associated with the development of ARF include nonsteroidal antiinflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, immunosuppressants (e.g., cyclosporine), antineoplastics (e.g., cisplatin), and antifungals (e.g., amphotericin B). The clinical course of ATN can be divided into the following three phases: oliguric (urine output of greater than 100 mL and less than 400 mL/day, lasting approximately 7-21 days), diuretic (7-14 days), and recovery (3-12 mo). Causes of intrinsic renal failure other than ATN include acute glomerulonephritis (GN), malignant hypertension, and hepatorenal syndrome.



Health care setting


Acute medical-surgical care unit



Assessment




Physical assessment:


Pallor, edema (peripheral, periorbital, sacral), jugular vein distention, crackles (rales), and elevated blood pressure (BP) in patient who has fluid overload.



Excess fluid volume:


Oliguria, pitting edema, hypertension, pulmonary edema.



Metabolic acidosis:


Kussmaul respirations (hyperventilation), lethargy, headache.



Electrolyte disturbance:


Muscle weakness and dysrhythmias.



Infection:


Urinary tract infection, septicemia, pulmonary infections, peritonitis.



Uremia (retention of metabolic wastes):


Altered mental state, anorexia, nausea, diarrhea, pale and sallow skin, purpura, decreased resistance to infection, anemia, fatigue. Note: Uremia adversely affects all body systems.



GI system:


Nausea, vomiting, diarrhea, constipation, gastrointestinal (GI) bleeding, anorexia, abdominal distention.



History of:


Exposure to nephrotoxic substances, recent blood transfusion, prolonged hypotensive episodes or decreased renal perfusion, sepsis, administration of radiolucent contrast media, or prostatic hypertrophy.



Diagnostic tests




Creatinine clearance:


Measures kidney’s ability to clear the blood of creatinine and approximates the glomerular filtration rate. It will decrease as renal function decreases. Creatinine clearance is normally decreased in older persons. Note: Failure to collect all urine during the period of study can invalidate the test.



Blood urea nitrogen (BUN) and serum creatinine:


Assess progression and management of ARF. Although both BUN and creatinine will increase as renal function decreases, creatinine is a better indicator of renal function because it is not affected by diet, hydration, or tissue catabolism.



Urinalysis:


Can provide information about cause and location of renal disease as reflected by abnormal urinary sediment (renal tubular cells and cell casts).



Urinary osmolality and urinary sodium levels:


To rule out renal perfusion problems (prerenal). In ATN, the kidney loses its ability to adjust urine concentration and conserve sodium, producing urine Na+ level greater than 40 mEq/L (in prerenal azotemia the urine Na+ is less than 20 mEq/L).


Note: All urine samples should be sent to the laboratory immediately after collection or should be refrigerated if this is not possible. Urine left at room temperature has greater potential for bacterial growth, turbidity, and alkalinity, any of which can distort the reading.



Renal ultrasound:


Provides information about renal anatomy and pelvic structures, evaluates renal masses, and detects obstruction and hydronephrosis. Because no intravenous (IV) contrast agent is used, this procedure limits risk of further compromise to renal function.



Renal scan:


Provides information about perfusion and function of the kidneys.



Computed tomography (CT) scan:


Identifies dilation of renal calices in obstructive processes.



Retrograde urography:


Assesses for postrenal causes (i.e., obstruction).





Nursing diagnosis:


Risk for infection

related to presence of uremia


Desired Outcome: Patient is free of infection as evidenced by normothermia; white blood cell (WBC) count 11,000/mm3 or less; urine that is clear and of normal odor; normal breath sounds; eupnea; and absence of erythema, warmth, tenderness, swelling, and drainage at the catheter or IV access sites.




Note:


One of the primary causes of death in ARF is sepsis.

























ASSESSMENT/INTERVENTIONS RATIONALES
Assess temperature and secretions for indicators of infection. Even minor increases in temperature can be significant because uremia masks the febrile response and inhibits the body’s ability to fight infection.
Use meticulous sterile technique when changing dressings or manipulating venous catheters, IV lines, or indwelling catheters. These measures prevent infection via spread of pathogens.
Avoid long-term use of indwelling urinary catheters. Whenever possible, use intermittent catheterization instead. Indwelling urinary catheters are a common source of infection.
Provide oral hygiene and skin care at frequent intervals. Intact skin and oral mucous membranes are barriers to infection.
Use emollients and gentle soap. These measures prevent drying and cracking of skin, which could lead to breakdown and infection.
Rinse off all soap when bathing patient. Soap residue may further irritate skin and affects its integrity.




Nursing diagnosis:


Ineffective protection

related to neurosensory, musculoskeletal, and cardiac changes occurring with uremia, electrolyte imbalance, and metabolic acidosis


Desired Outcomes: After treatment, patient verbalizes orientation to person, place, and time and is free of injury caused by neurosensory, musculoskeletal, or cardiac disturbances. Within the 24-hr period before hospital discharge, patient verbalizes signs and symptoms of electrolyte imbalance and metabolic acidosis and importance of reporting them promptly should they occur.










ASSESSMENT/INTERVENTIONS RATIONALES
Assess for and alert patient to indicators of alterations in fluid, electrolyte, and acid-base balance.
In ARF, the kidneys lose the ability to maintain biochemical homeostasis, causing retention of metabolic wastes and dramatic alterations in fluid, electrolyte, and acid-base balance. The following may occur:
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Acute renal failure

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