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Acute Renal Failure ( ARF ) - is a rapid loss of renal function due to damage of the kidneys. - depending on the duration and severity, a wide range of potentially life-threatening metabolic complications can occur.
Categories of ARF
When reductions in renal blood flow interrupt glomerular pressure; the result is the development of acute renal failure. Prerenal ARF occurs in 60% to 70% of cases - result of impaired blood flow that leads to hypoperfusion of the kidney and a decrease in the GFR.
Intrarenal ARF anything that causes direct insult to the kidneys. - Acute tubular necrosis (ATN) is the most common type of intrarenal ARF. Characteristics of ATN:
Intratubular Obstruction Tubular back leak vasoconstriction Changes in glomerular permeability
Postrenal ATF results from obstruction distal to the kidney. pressure rises in the kidney tubules and eventually, the GRF .
Causes of ARF
1. Prerenal Failure - volume depletion - impaired cardiac efficiency - vasodilation 2. Intrarenal Failure - prolonged renal ischemia - nephrotoxic agents - infectious processes
Phases of ARF
1. Initiation begins with the initial insult
and ends with oliguria develops. This phase can last from hours to days and is characterized by:
Renal flow at 25% of normal Oxygenation to the tissue at 25% of normal Urine output at 30 ml (or less) per hour Urine sodium excretion greater than 40 mEq/L.
Pathophysiology
decline in renal blood flow (RBF)
decreased glomerular filtration causes tissue ischemia and eventually cell necrosis or cell death produces oxygen free radicals and other enzymes which exacerbate the problem sloughing of cells which in turn block renal tubules and cause a back leak of glomerular filtrate
Assessment History
Changes in the urine output - varies from scanty to a normal volume - hematuria may be present - urine has low specific gravity - inability to concentrate urine early manifestation of tubular damage - prerenal azotemia: amount of Na in the urine normal urinary sediment -intrarenal azotemia: amount of Na in urine with urinary cast and cellular debris
BUN level - steadily at a rate dependent on the degree of catabolism, renal perfusion, protein intake Creatinine level - useful in monitoring kidney function
Assess pts for hyperkalemia - may lead to dysrhythmias, such as ventricular tachycardia and cardiac arrest Progressive metabolic acidosis - cannot eliminate metabolic load of acidtype substances produced by the normal metabolic processes
There may be an increase in blood phosphate concentrations Calciums level may be low Anemia as a result of reduced erythropoietin production, uremic GI lesions, reduced RBC lifespan and blood loss from the GI tract
Diagnostic studies
- ultrasonography effective in determining existing renal failure and/or obstruction of the urinary collecting system - CT or MRI scan may show evidence of anatomic changes -Creatinine Clearance Test this is believed to be the most accurate test to determine glomerular filtration rates - blood exam
- urinalysis - renal biopsy only be done if the result will alter the treatment plan