Acute Kidney Injur_Elimination_Student_2024.pptx

Acute Kidney Injury (Acute Renal Failure), Burns, Renal Calculi, & Fissures NRSG3301 C RY S TA L T R E I G E M N N P Concept(s) & Exemplar(s) Concept(s): Fluid & electrolytes Elimination Exemplar(s): Acute kidney injury (AKI) Burns Renal calculi, fissures Acute Kidney Injury Acute kidney inj...

Acute Kidney Injury (Acute Renal Failure), Burns, Renal Calculi, & Fissures NRSG3301 C RY S TA L T R E I G E M N N P Concept(s) & Exemplar(s) Concept(s): Fluid & electrolytes Elimination Exemplar(s): Acute kidney injury (AKI) Burns Renal calculi, fissures Acute Kidney Injury Acute kidney injury (AKI) refers to an abrupt decrease in kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes. The term AKI has largely replaced acute renal failure (ARF), reflecting the recognition that smaller decrements in kidney function that do not result in overt organ failure are of substantial clinical relevance and are associated with increased morbidity and mortality (UTD, 2023) Kidneys - primary organs for regulating fluid and electrolyte balance Kidneys regulate water balance by adjusting urine volume Urinary excretion of most electrolytes - adjusted so a balance is sustained between intake and output (Evolve, 2023) Acute Kidney Injury Kidneys Total plasma volume-filtered by the kidneys many times each day; average adult-kidneys reabsorb 99% of this filtrate- produces about 1.5 L of urine per day Filtrate moves through renal tubules-selective reabsorption of water and electrolytes, secretion of electrolytes lead to the formation of urine Process-aids in maintaining normal plasma osmolality, electrolyte balance, blood volume, acid–base balance Renal tubules-area where ADH, aldosterone work (Evolve, 2023) Acute Kidney Injury Renal (injury) failure-partially or complete cessation of kidney function Acute kidney injury (AKI) is associated with a loss of renal function over a few days and can typically be reversed (Evolve, 2023) Acute Kidney Injury Diagnostic criteria-Acute reduction in urine output, elevation in serum creatinine, or both Can have Azotemia-accumulation of nitrogen waste products (urea nitrogen, creatinine) in the blood Untreated kidney injury-fluid overload, electrolyte imbalances, metabolic acidosis, leads to(Evolve, death 2023) due to infection Acute Kidney Injury AKI-severe causes include prolonged hypotension or hypovolemia or exposure to a nephrotoxic agent Acute kidney injury develops over hours or days with increases in elevations of blood urea nitrogen (BUN), creatinine, potassium, with or without oliguria Severe AKI develops in over 60% of critical care (Evolve, unit 2023) (CCU) patients-mortality rates of 70 to 80% Acute Kidney Injury Commonly used classification systems for AKI- uses serum creatinine, glomerular filtration rate (GFR *size, age sex compared to serum Creat levels), urine output to identify risk, injury, failure, loss, end- stage kidney disease (the RIFLE criteria) Diagnosis (CPG, 2018) RIFLE Criteria (CPG, 2018) Acute Kidney Injury Age Considerations: Older persons-more susceptible than younger adults to AKI- number of functioning nephrons decreases with age Impaired function of other organ systems (e.g., cardiovascular disease, impaired pancreas function * hypoxemia, release of pancreatic amylase etc.) can increase the risk of developing AKI Aging kidney is less able to compensate for changes in fluid (Evolve, 2023) volume, solute load, cardiac output AKI: Classification Causes of acute kidney injury AKI classified as: Prerenal Renal Postrenal Prerenal AKI is due to inadequate renal perfusion. The main causes are Extracellular fluid volume depletion (eg, due to inadequate fluid intake, diarrheal illness, sepsis) Cardiovascular disease (eg, heart failure, cardiogenic shock) Decompensated liver disease Prerenal conditions typically do not cause permanent kidney damage (and hence are potentially reversible) unless hypoperfusion is severe and/or prolonged. Hypoperfusion of an otherwise functioning kidney leads to enhanced reabsorption of sodium and water, resulting in oliguria (urine output < 500 mL/day) with high urine osmolality and low urine sodium (Merck, 2023) AKI: Classification Renal causes of AKI involve intrinsic kidney disease or damage. Disorders may involve the blood vessels, glomeruli, tubules, or interstitium. The most common causes are: Acute tubular necrosis Acute glomerulonephritis Nephrotoxins (including prescription and over-the-counter drugs (eg. Antibiotics such as aminoglycosides, cephalosporins, diuretics, etc.) Glomerular disease reduces glomerular filtration rate (GFR) and increases glomerular capillary permeability to proteins and red blood cells; it may be inflammatory (glomerulonephritis) or the result of vascular damage due to ischemia or vasculitis Tubules also may be damaged by ischemia and may become obstructed by cellular debris, protein or crystal deposition, and cellular or interstitial edema. Interstitial inflammation (nephritis) usually involves an immunologic or allergic phenomenon. These mechanisms of tubular damage are complex and interdependent, rendering the previously popular term acute tubular necrosis an inadequate description (Merck, 2023) AKI: Classification Postrenal AKI (obstructive nephropathy) is due to various types of obstruction in the voiding and collecting parts of the urinary system. Obstruction can also occur on the microscopic level within the tubules when crystalline or proteinaceous material precipitates. Obstructed ultrafiltrate, in tubules or more distally, increases pressure in the urinary space of the glomerulus, reducing GFR. Obstruction also affects renal blood flow, initially increasing the flow and pressure in the glomerular capillary by reducing afferent arteriolar resistance. However, within 3 to 4 hours, the renal blood flow is reduced, and by 24 hours, it has fallen to < 50% of normal because of increased resistance of the renal vasculature. Renovascular resistance may take up to a week to return to normal after relief of a 24-hour obstruction. To produce significant AKI, obstruction at the level of the ureter requires involvement of both ureters unless the patient has only a single functioning kidney. Bladder outlet obstruction due to an enlarged prostate is probably the most common cause of sudden, and often total, cessation of urinary output in men (Merck, 2023) Acute Kidney Injury Initially, weight gain and peripheral edema may be the only findings Symptoms of uremia may develop later as nitrogenous products accumulate. Such symptoms include Anorexia Nausea Vomiting Weakness Myoclonic jerks Seizures Confusion Coma ***Asterixis and hyperreflexia may be present on examination. Chest pain (typically worse with inspiration or when recumbent), a pericardial friction rub, and findings of pericardial tamponade may occur if uremic pericarditis is present. Fluid accumulation in the lungs may cause dyspnea and crackles on auscultation (Merck, 2023) Acute Kidney Injury Three phases of urine output: Prodromal phase - usually has normal urine output and varies in duration depending on causative factors (eg, the amount of toxin ingested, the duration and severity of hypotension). Oliguric phase - has urine output typically between 50 and 500 mL/day. The duration of the oliguric phase is unpredictable, depending on etiology of AKI and time to treatment. However, many patients are never oliguric. Nonoliguric patients have lower mortality and morbidity and less need for dialysis. Postoliguric phase - urine output gradually returns to normal, but serum creatinine and urea levels may not fall for several more days. Tubular dysfunction may persist for a few days or weeks and is manifested by sodium wasting, polyuria (possibly massive) unresponsive to vasopressin, or hyperchloremic metabolic acidosis. (Merck, 2023) Acute Kidney Injury Diagnosis: Based on clinical evaluation, medication review (including all OTC/herbal remedies/etc.), review of recent exposures eg. Iodinated IV contrast media Laboratory testing : CBC, BUN, serum creatinine, electrolytes, calcium, phosphate Urinary sediment Urinary diagnostics (sodium, urea, protein, creatinine concentration) Urinalysis and assessment of urine protein Postvoid residual bladder volume and/or renal ultrasound if postrenal cause suspected (Merck, 2023) Acute Kidney Injury Results may include: Progressing acidosis Hyperkalemia Hyponatremia (usually moderate and correlates with a surplus of dietary or intravenous water intake Anemia (normochromic/normocytic) Hyperphosphatemia Hypocalcemia (Merck, 2023) Acute Kidney Injury: Determining Cause Priority is to rule out reversible causes first (eg. Extracellular fluid (ECF) volume depletion & obstruction). Review all medications and stop any renal toxic drugs Prerenal – often clinically apparent, treat the underlying cause (eg. in hypovolemia, volume infusion can be tried; in heart failure (HF), diuretics and afterload-reducing drugs can be tried). Improving of AKI confirms a prerenal cause. Renal – often diagnosed on clinical findings such as edema (glomerulonephritis), proteinuria (nephrotic syndrome) Postrenal – after the patient voids U/S bladder completed (or in-out catheter) to measure post-void residual urine amount, >200ml is suggestive of bladder outlet obstruction or weakened bladder muscles. (Merck, 2023) AKI: Treatment May require immediate treatment for life-threatening conditions (pulmonary edema, hyperkalemia) Medication adjustments as needed (eg. Adjusting antibiotic dose) May require fluid restriction (sodium, phosphate, potassium intake) May require dialysis (Merck, 2023) Acute Kidney Injury Urgent Indications for kidney replacement therapy (dialysis): Fluid overload refractory to diuretic therapy Severe hyperkalemia (plasma concentration >6.5mEq/L) or rapidly rising potassium levels Overt manifestations of uremia, such as pericarditis, encephalopathy, or an otherwise unexplained decline in mental status Severe metabolic acidosis (ph Women 50% recurrence (lifestyle factors) >in summer > family history Many factors affect the incidence and the type of stone formation, including metabolic, dietary, genetic, climatic, lifestyle, and occupational influences Various theories have been proposed to explain the formation of stones in the urinary tract; however, no single theory can account for stone formation in all cases (Evolve, 2023) RISK FACTORS FOR THE DEVELOPMENT OF URINARY TRACT CALCULI Metabolic Diet Abnormalities that result in increased Excessive amounts of tea or fruit juices urine levels of calcium, oxaluric acid, uric that elevate urinary oxalate level acid, or citric acid Large intake of calcium* and oxalate (peanuts, rhubarb, spinach, beets, chocolate and sweet potatoes) Climate Warm climates that cause increased Large intake of dietary proteins that fluid loss, low urine volume, and increased increase uric acid excretion solute concentration in urine Low fluid intake that increases urinary concentration Lifestyle Sedentary occupation, immobility Genetic Family history of stone formation, cystinuria, gout, or renal acidosis Urinary Tract Calculi (Cont.) Infected stones, when they are entrapped in the kidney, may assume a staghorn configuration as they enlarge Infected stones are frequent in patients with an external urinary diversion, long-term in-dwelling catheter, neurogenic bladder, or urinary retention (Evolve, 2023) 68  Stone Types Calcium Calcium Struvite Uric Acid Cystine Oxlate Phosphate 35-40 % 8-10% 10-15% 5-8% 1-2% Small Mixed >women >men Genetic Ureter stones Frequent Gout, defect, >Men Alkaline UTI acidic cysteine Urine urine, not inherited absorbed in GI or kidney Acidic Urine Assessment Pain 0-10 (usually 10) abdominal (bladder) or flank (upper ureter) Hematuria Nausea and vomiting Moist cool skin May feel pain in testes or labia Urinary stones cause clinical manifestations when they obstruct urinary flow (Lewis, 2019) Implementation DIAGNOSTICS TREATMENT UA Urine C&S Pain management (obstructive) IVP (KUB) Treat infection (struvite) Retrograde pyelogram Assess and evaluate symptoms of infection Renal US Strain urine Evaluate the cause of stone formation to Cystoscopy prevent further development of stones. CT Pre-op prep and education if applicable Urinary Tract Calculi Collaborative care Lithotripsy (larger stones) Surgical therapy >4mm usually need surgery Cystoscopy Small stones in bladder Nutritional therapy advice ◦ Purine (sardines, liver kidney, venison, goose) ◦ Calcium (milk, cheese beans ,lentils, dried fruit, chocolate) ◦ Oxalate (spinach, rhubarb, tomatoes, beets, nuts, Worcestershire) (Lewis, 2019) Copyright © 2019 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. 77 Goals of care (1) relief of pain, (2) no urinary tract obstruction, (3) an understanding of measures to prevent further recurrence of stones. *** To prevent stone recurrence, the patient should consume an adequate fluid intake to produce a urine output of approximately 2 L/day. Additional preventive measures focus on reducing metabolic or secondary risk factors (e.g., restricting dietary purines, oxalate and calcium). (Lewis, 2019)