Acute Kidney Injury (AKI) PDF

ACUTE KIDNEY INJURY ACUTE KIDNEY INJURY (AKI) Previously known as acute kidney failure (AKF) or acute renal failure (ARF) Potentially reversible Rapid loss of kidney function Rapid and progressive azotemia Possible uremia Oliguria AKI- CATEGORIES Prerenal Intrarenal Postrenal Table 46.2 in Lewis PRE...

ACUTE KIDNEY INJURY ACUTE KIDNEY INJURY (AKI) Previously known as acute kidney failure (AKF) or acute renal failure (ARF) Potentially reversible Rapid loss of kidney function Rapid and progressive azotemia Possible uremia Oliguria AKI- CATEGORIES Prerenal Intrarenal Postrenal Table 46.2 in Lewis PRERENAL CAUSES OF AKI Result of external factors that reduce renal blood flow Decreased glomerular perfusion Decreased filtration of the kidneys Usually no parenchymal damage PRERENAL CAUSES- EXAMPLES Hypovolemia Decreased Cardiac Output Vasodilation Decreased Peripheral Vascular Resistance Decreased Renovascular Blood Flow INTRARENAL CAUSES OF AKI Results of conditions that cause direct damage to the parenchyma Impaired nephron function Structural and functional changes within the kidney INTRARENAL CAUSES- EXAMPLES Acute Tubular Necrosis (ATN) Most common intrarenal cause of AKI Responsible for 90% of intrarenal AKI cases Severe kidney ischemia causes a disruption in the basement membrane and destruction of the tubular epithelium Nephrotoxic agents cause necrosis of tubular epithelial cells, which slough off and plug the tubules Risks associated with development of ATN include Major surgery, shock, sepsis, blood transfusion reaction, muscle injury from trauma, prolonged hypotension and nephrotoxic agents ATN is reversible INTRARENAL CAUSES- EXAMPLES Acute Glomerulonephritis: Inflammation of glomeruli Acute Interstitial Nephritis: Inflammation of kidney’s interstitial tissues Acute Vascular Disorders: Conditions affecting blood vessels within the kidney Other Causes: Prerenal aki, toxemia of pregnancy, malignant hypertension, Systemic Lupus Erythematosus POSTRENAL CAUSES OF AKI Involve mechanical obstruction of the lower urinary tract Ureters, bladder, urethra Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation) Kidney dilation leads to an increase in hydrostatic pressure and tubular blockage causing a progressive decline in kidney function If relieved in 48 hours of onset recovery is likely After 12 weeks recovery is unlikely Fewer than 5% of all cases of AKI POSTRENAL CAUSES- EXAMPLES Benign Prostatic Hyperplasia (BPH) Bladder cancer Prostate cancer Neuromuscular disorders Calculi formation (stones) Trauma (back, pelvis, perineum) Spinal cord disease Extrarenal tumors LAB VALUES RELATED TO KIDNEY FUNCTION GFR- Glomerular filtration rate 125 mL/min Serum creatinine 0.6-1.3 mg/dL BUN- Blood urea nitrogen 8-21 mg/dL CLINICAL MANIFESTATIONS 3 Phases of AKI progression Oliguric Diuretic Recovery OLIGURIC PHASE Reduction in urine output to < 400 mL/24 hrs (Oliguria) Onset occurs within 1-7 days of kidney injury, lasts 10-14 days or longer Decreased urine output > increased fluid retention. JVD, edema, hypertension, heart failure, pulmonary edema 50% of patients are non-oliguric Interstitial nephritis ATN Anuria Urinary tract obstruction OLIGURIC PHASE Metabolic Acidosis Serum bicarbonate level drops Severe acidosis- patient may develop Kussmaul respirations Sodium balance Damaged tubules cannot conserve sodium Normal or below normal level of serum sodium Hyperkalemia Hematologic disorders Leukocytosis, infection Waste Product Accumulation BUN and serum creatinine levels are increased. **** an elevated BUN level can also be caused by dehydration, corticosteroids, etc. Neurologic disorders Mild – fatigue, difficulty concentrating. Severe- seizures, stupor and coma. Asterixis (flapping tremor with the wrist extended) – common with liver failure, also occurs with severe kidney failure. DIURETIC PHASE Daily urine output 1-3 liters per day High volume output Inability of the tubules to concentrate the urine Hypovolemia and hypotension can occur Uremic symptoms start to improve Monitor the patient Sodium imbalance, hypokalemia, and dehydration RECOVERY PHASE GFR increases Serum creatinine and BUN levels decrease (normalize) Urine output normalizes 1-2 weeks in this phase to improve, but can be 12 months to stabilize Some patients never recover (older less likely) Outcome influenced by: Patient’s overall health Severity of kidney failure Number/types of complications DIAGNOSTICS History Identify precipitating cause Change in urine output Serum creatinine, BUN levels, GFR Serum electrolytes Urinalysis Renal ultrasound Renal scan CT scan Renal biopsy –best method to confirm intrarenal cause INTERPROFESSIONAL CARE Goal Eliminate the cause Manage signs and symptoms Prevent complications while the kidneys recover Conservative therapy Maintain adequate intravascular volume Diuretics (furosemide, bumetanide, mannitol) Monitor fluid intake and calculate fluid restriction Losses (mL) + 600mL = amount of fluid intake for the day Manage hyperkalemia Renal Replacement Therapy (RRT) INTERPROFESSIONAL CARE Nutrition Therapy Provide adequate calories to prevent further breakdown of body protein for energy purposes Carbohydrates, protein and fat with supplemental amino acids 30-40% of calories should be from fat Strict sodium and potassium regulation Phosphorus regulation INTERPROFESSIONAL CARE Hyperkalemia treatment: Stabilize myocardial cell membrane IV calcium gluconate Enhance cellular uptake of potassium IV glucose followed by IV regular insulin Albuterol and bicarbonate (not first line of tx) Enhance total body elimination of K Sodium polystyrene sulfonate (Kayexalate) IV furosemide (Lasix) Emergent hemodialysis NURSING MANAGEMENT Monitor vital signs Monitor intake and output Monitor for fluid volume overload Monitor lab values Lung sounds Monitor patients taking potentially nephrotoxic medications (include NSAIDs) Monitor daily weights Strict aseptic technique Skin care Mouth care to prevent stomatitis (develops when ammonia irritates the mucous membranes) CHRONIC KIDNEY DISEASE