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## Post-procedure: - Maintain patient in prone position immediately after procedure and on bedrest for 6 to 8 hours. Monitor urine for hematuria and compare with pre-op specimen. - Monitor VS every 5 to 15 minutes for first hour and then less frequently, noting hypotension, tachycardia - Note anor...

## Post-procedure: - Maintain patient in prone position immediately after procedure and on bedrest for 6 to 8 hours. Monitor urine for hematuria and compare with pre-op specimen. - Monitor VS every 5 to 15 minutes for first hour and then less frequently, noting hypotension, tachycardia - Note anorexia, vomiting, abdominal discomfort that suggest bleeding - Note pain: Severe colicky pain may indicate clot in the ureter - Obtain hemoglobin and hematocrit levels within 8 hours - Maintain fluid intake at 3000 mL/day in absence of renal insufficiency - Provide blood component therapy and surgical repair if bleeding occurs ## ATN Acute tubular necrosis (ATN) occurs when a hypoxic condition causes renal ischemia that damages tubular cells of the glomeruli so they are unable to adequately filter the urine, leading to acute renal failure. Causes include hypotension, hyperbilirubinemia, sepsis, surgery (especially cardiac or vascular), and birth complications. ATN may result from nephrotoxic injury related to obstruction or drugs, such as chemotherapy, acyclovir, and antibiotics, such as sulfonamides and streptomycin. Symptoms may be non-specific initially and include life-threatening complications: - Lethargy - Nausea and vomiting - Hypovolemia with low cardiac output and generalized vasodilation - Fluid and electrolyte imbalance leading to hypertension, CNS abnormalities, metabolic acidosis, arrhythmias, edema, and congestive heart failure - Uremia leading to destruction of platelets and bleeding, neurological deficits, and disseminated intravascular coagulopathy (DIC) ## Treatment includes: - Identifying and treating underlying cause - Supportive care - Loop diuretics (in some cases), such as Lasix® - Antibiotics for infection - Discontinuation of nephrotoxic agents - Kidney dialysis - Infections can include pericarditis & sepsis ## Chronic Renal Failure Chronic renal failure, which progresses to end-stage renal disease, occurs when the kidneys are unable to filter and excrete wastes, concentrate urine, and maintain electrolyte balance because of hypoxic conditions, kidney disease, or obstruction in the urinary tract. It results first in azotemia (increase in nitrogenous waste in the blood) and then in uremia (nitrogenous wastes cause toxic symptoms). When >50% of the functional renal capacity is destroyed, the kidneys can no longer carry out necessary functions and progressive deterioration begins over months or years. In children, chronic renal failure is associated developmental kidney defects, hereditary diseases, infections, glomerulonephritis, or progression of nephrotic syndrome. The child may initially show few symptoms, but the child becomes increasingly weak and lethargic with a multiplicity of symptoms affecting most body systems. Chronic renal failure is not reversible, so treatment aims to