【持续性肾脏替代治疗crrt英文精品课件】acute renal failure (106p)

Acute Renal Failure,Chapter 45,Abbreviations,ARF: acute renal failure ATN: acute tubular necrosis BUN: blood urea nitrogen CKD: chronic kidney disease CLcr: creatinine clearance CRRT: continuous renal replacement therapy CT: computed tomography CVVH: continuous venovenous hemofiltration CVVHD: continuous venovenous hemodialysis CVVHDF: continuous venovenous hemodiafiltration FENa: fractional excretion of sodium GFR: glomerular filtration rate IHD: intermittent hemodialysis NSAID: nonsteroidal antiinflammatory drug QALY: quality-adjusted life-year RRT: renal replacement therapy Scr: serum creatinine,Key Concepts,Acute renal failure (ARF) is a common complication in hospitalized patients associated with high mortality ARF categorized based on anatomic area of injury or malfunction prerenal intrinsic postrenal,3,Key Concepts,ARF risk factors advanced age acute infection preexisting chronic respiratory or cardiovascular disease dehydration chronic kidney disease ARF lacks a specific/sensitive sign to herald onset Prevention is key Supportive management primary approach to preventing/reducing complications,4,Acute Renal Failure: Definition,Decrease in glomerular filtration rate (GFR) associated with accumulation of waste products, including urea and creatinine relatively abrupt decline in renal function No universally accepted definition Clinicians use some combination of absolute Scr value, change in Scr value over time, and/or urine output as primary diagnostic criteria,5,Acute Renal Failure: Definition,Consensus-derived definition and ARF classification system 3-tiered classification uses GFR and urine output plus 2 clinical outcomes that may occur subsequent to an ARF episode RIFLE risk of dysfunction (R) injury to the kidney (I) failure of the kidney (F) loss of function (L) end-stage renal disease (E),6,7,ESRD, end-stage renal disease GFR, glomerular filtration rate Scr, serum creatinine,RIFLE classification,ARF Epidemiology,Uncommon condition in healthy population annual incidence 0.02% Incidence as high as 13% in patients with preexisting CKD Hospitalized patients high risk of ARF (incidence 7%) Incidence higher in critically ill patients (6% to 23%),8,Lameire N, Van Biesen WV, Vanholder R. The changing epidemiology of ARF. Nat Clin Prac Nephrol 2006;2:364377.,Pruchnicki MC, Dasta JF. Acute renal failure in hospitalized patients: Part I. Ann Pharmacother 2002;36:12611267.,Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002;39:930936.,Incidence and Outcomes of Acute Renal Failure Relative to Where It Occurs,9,Etiology,ARF categorized based on anatomic location of injury associated with precipitating factor(s) prerenal: due to decreased renal perfusion in setting of undamaged parenchymal tissue intrinsic: result of structural kidney damage, most commonly tubule from ischemic or toxic insult postrenal: caused by obstruction of urine flow downstream from the kidney,10,11,Etiology,Community-Acquired Secondary to renal hypoperfusion from volume depletion, heart failure, or medications Hospital- and ICU-Acquired Ischemic or toxic acute tubular necrosis (ATN),12,13,Pathophysiology,Pseudorenal and Functional ARF,Pseudorenal ARF rise in either blood urea nitrogen (BUN) or Scr suggests renal dysfunction when GFR not diminished Functional ARF decline in GFR secondary to reduced glomerular hydrostatic pressure (driving force for ultrafiltrate formation) can occur without damage to the kidney itself may be due to changes in glomerular afferent (vasoconstriction) and efferent (vasodilation) arteriolar circumference,14,Prerenal Acute Renal Failure,Hypoperfusion of renal parenchyma + systemic arterial hypotension Concurrent systemic hypotension caused by decline in intravascular or effective blood volume hemorrhage dehydration hypoalbuminemia diuretic therapy No systemic hypotension: possibly due to renal artery occlusion; atherosclerosis is a common cause,15,Intrinsic Acute Renal Failure,Damage to the kidney itself Categorized by injured structure within the kidney renal vasculature (uncommon) occlusion of renal vessels glomeruli (5%) tubules (85% caused by ATN) interstitium acute interstitial nephritis (AIN),16,Postrenal Acute Renal Failure,May result from obstruction at any level in the urinary collection system from the renal tubule to urethra if obstructing process above the bladder, it must involve both kidneys or one kidney in a patient with a single functioning kidney to cause significant ARF bladder outlet obstruction neurogenic bladder or anticholinergic medications chemotherapy-induced tumor lysis syndrome,17,Diagnosis,ARF signs and symptom highly variable, depending on etiology Determine if renal complication is acute, chronic, or result of acute changes in a CKD patient,18,Patient Assessment,Past medical history to differentiate between acute and chronic renal failure Medication and recent procedure history may suggest causes for acute interstitial nephritis or other nephrotoxic effects Medications diuretics NSAIDs antihypertensives contrast dye other recent additions or changes,19,Patient Assessment,Patients may have acute change in voiding habits Onset of flank pain urinary stone Severe headaches severe hypertension as result of ARF,20,Patient Assessment,Patients who develop renal insufficiency while hospitalized usually have acute initiating event identified from laboratory data, urine output record, medication administration records, procedure records Acute anuria: caused by complete urinary obstruction or catastrophic event (shock, acute cortical necrosis) Oliguria (urine output 500 mL/day) acute intrinsic renal failure, incomplete urinary obstruction,21,Signs and Symptoms,Edema Colored or foamy urine Orthostatic hypotension in volume-depleted patients Hypertension in fluid-overloaded patients or presence of acute or chronic hypertensive kidney disease Outpatient: change in urinary habits, sudden weight gain, flank pain Inpatient: typically recognized by clinicians before the patient; may not experience obvious symptoms,22,Laboratory Tests,Elevations in serum potassium, BUN, creatinine, phosphorous, or reduction in calcium and pH (acidosis) Sepsis-associated ARF: increased WBC count ATN: eosinophilia Urine microscopy: cells, casts, crystals help distinguish among possible etiologies and/or ARF severities Elevated urine specific gravity suggests prerenal ARF, as tubules are concentrating urine Urine chemistry protein glomerular injury blood damage to any kidney structure,23,Other Diagnostic Tests,Renal ultrasonography or cystoscopy to rule out obstruction Renal biopsy rarely used; reserved for difficult diagnoses,24,Clinical Presentation,Acute interstitial nephritis patients frequently unable to concentrate urinary solutes Evaluate blood pressure for elevations that may accompany intrinsic renal damage recent infection postinfective glomerulonephritis Physical examination may detect possible postrenal obstruction urinary catheter enlarged prostate in males cervical/uterine abnormalities in females Renal artery stenosis identified via ultrasound,25,Laboratory Test Interpretation,No consensus on degree and time frame of Scr changes Abrupt cessation in glomerular filtration will not yield immediate measurable Scr change creatinine generation and accumulation relatively slow lag time between test and clinical event lab tests may not be sensitive to small GFR changes, and fluid retention that commonly accompanies ARF dilutes retained creatinine when decreased filtration of creatinine occurs, functional tubules increase secretion of creatinine into urine further complicating Scr interpretation,26,27,Glomerular filtration rate (GFR; mL/min) and serum creatinine (Scr; g/dL) versus time following acute renal injury. Prior to time 0, a GFR of 120 mL/min and a Scr of 1.0 g/dL exist. At time 0, an abrupt renal artery thrombus forms, depriving one kidney of renal blood flow. Composite GFR immediately declines by 50% to approximately 60 mL/min. However, Scr does not increase immediately, as it is dependent on creatinine production and attainment of steady-state serum concentrations.,Laboratory Test Interpretation,Cockcroft-Gault or Modification of Diet in Renal Disease equations estimate GFR in CKD patients not applicable for ARF patients with changing Scr values renal function unstable these equations can overestimate GFR when ARF is worsening and underestimate GFR when ARF is resolving Look at sequence of Scr values to determine if renal function is improving (values declining) or worsening (values rising),28,Laboratory Test Interpretation,Urine output assists in verifying observed serum laboratory values up-to-the-moment means of identifying changes dependent on hydration status, medications Anuria (urine output 17 mL/h) despite reasonable urine output, urine not composed of expected waste products and solutes,29,Laboratory Test Interpretation,Damaged tubules may allow substantial urine production kidney electrolyte, protein, acidbase functions may be severely compromised Urine output alone unreliable marker of kidney function BUN to Scr ratio normal renal function: 20:1 reabsorption of BUN exceeds that of creatinine,30,Laboratory Test Interpretation,High urinary specific gravity (in absence of glucosuria or mannitol administration): intact urinary concentrating mechanism ARF likely prerenal Proteinuria: glomerular damage Hematuria: acute intrinsic ARF secondary to glomerular or injury to other tissue Crystals: nephrolithiasis and postrenal obstruction WBC or WBC casts: interstitial inflammation,31,Laboratory Test Interpretation,Measurement of urine and serum electrolytes helpful in ARF calculate fractional excretion of sodium FeNa = (UNa x Scr x 100)/(Una x SNa) Prerenal azotemia low urinary sodium concentration ( 500 mOsm/L) suggests stimulation of antidiuretic hormone and intact tubular function Tubular damage: inability to concentrate urine results in high fractional excretion of sodium ( 2%),32,Differentiating ARF Causes,33,Urine Analysis as Guide to ARF Etiology,34,Differential Diagnosis of ARF on Basis of Urine Microscopic Examination Findings,35,Novel Biomarkers,Allows for significantly earlier diagnosis of AKI 48 hrs before a rise in SCr is observed Serum cystatin C Neutrophil gelatinase-associated lipocalin (NGAL) Kidney injury molecule 1 (KIM-1) Interleukin (IL-18) Liver-type fatty acid binding protein (L-FABP) Beta trace protein (BTP),36,Diagnostic Procedures,If urinary catheter insertion into patients bladder after voiding or attempt to void does not yield 500 mL of urine exclude postrenal obstruction distal to the bladder as ARF cause Renal biopsies used when ARF cause not evident risk of bleeding performed only when definitive diagnosis needed to guide therapy, such as precise etiology of glomerulonephritis,37,38,Prevention of ARF,Desired Outcome,Prevention is critical Goals prevent ARF avoid/minimize further renal insults that would worsen existing injury or delay recovery provide supportive measures until kidney function returns,39,Desired Outcome,Preventative strategies useful in predictable cases decreased perfusion secondary to abdominal surgery coronary bypass surgery acute blood loss in trauma uric acid nephropathy When patients with ARF risk factors are scheduled for surgery, clinicians should know the likelihood of the patient developing ARF is high and consider preventative measures discontinue medications that may increase likelihood of renal damage (NSAIDs, ACE inhibitors),40,Prevention,Evaluate fluid balance: measure acute changes in weight, blood pressure Educate patient on preventative measures Treatment that can pose a risk for insult to the kidney (e.g., chemotherapy or uric acid nephropathy) Teach patients about optimal daily fluid intake (2 L/day) History of nephrolithiasis: dietary restrictions, depending on type of stones in the past Foley catheter: proper care and monitoring to prevent post-obstructive ARF,41,Prevention of AKI,42,Nonpharmacologic Therapies,Contrast-induced nephropathy (CIN) Hydration isotonic saline: 1 mgL/kg/hr for 12 hrs before and 12 hrs after procedure sodium bicarbonate: 154 mEq/L infused at 3 mL/kg/hr for 1 hr before procedure and 1 mL/kg/hr for 6 hrs after procedure Extracorporeal blood purification prophylactic RRT current data does not demonstrate consistent significant benefit,43,Nonpharmacologic Therapies,Administration, rate, formulation changes in cases when nephrotoxic agent use cannot be avoided Example: amphotericin B to treat fungal infections highly nephrotoxic causes ARF in 30% of patients reduce nephrotoxic potential by slowing infusion rate from 4-hours to a 24-hour infusion of same dose use liposomal forms in patients with ARF risk factors more expensive lower incidence of kidney damage,44,Pharmacologic Therapies,Loop diuretics Dopamine Agonists Antioxidants: ascorbic acid and N-acetylcysteine Other therapies: theophylline, erythropoietin alfa (EPO), natriuretic peptides,45,Loop Diuretics,Early experimental studies proposed theoretical advantages but clinical studies less favorable Increased urine output but lack beneficial effects on patient outcomes Some evidence of potential harm,46,Clinical Controversy,Loop diuretics are widely used for the management of volume overload in critically ill patients (including those with concomitant AKI) Volume overload is an appropriate indication for loop diuretics, but current evidence does not support their use in prevention of AKI or treatment of oliguria,Dopamine Agonists,Theoretical benefits: low doses of IV dopamine (2 mcg/kg/min) should renal blood flow and induce natriuresis and diuresis Controlled studies have not supported theories dopamine 2 mcg/kg/min worsened renal perfusion indices compared to saline in a crossover study in ARF patients Current evidence does not support use of low-dose dopamine for prevention of AKI,48,Clinical Controversy,Despite most studies not showing improved patient outcomes with its use, low-dose dopamine is still commonly used Risks associated with dopamine use (extravasation and potential dosing errors) suggest it should be avoided whenever possible Meta-analysis of low-dose dopamine studies from 1966 to 2000 concluded low-dose dopamine does not prevent ARF and its use cannot be justified,Antioxidants,Ascorbic acid Studied in prevention of CIN Antioxidant properties thought to alleviate oxidative stress caused by CIN-associated ischemia reperfusion injury Studies have not consistently demonstrated benefit Excellent safety profile option for high-risk patients,50,Antioxidants,N-Acetylcysteine Therapeutic benefit not consistently demonstrated Low cost, safety profile, tolerability, and possible benefit make it a reasonable option in high-risk patients Should only be reserved for prevention of CIN and not other types of AKI,51,Other Agents,Theopyhlline may reduce CIN incidence with efficacy comparable to N-acetylcysteine inconsistent findings across studies evidence currently inconclusive and more research is needed Erythropoietin alfa (EPO) small prospective randomized trial showed decreased risk of post-op AKI recent double-blind placeb0-controlled trial found no difference need larger clinical trials to demonstrate safety and efficacy,52,Other Agents,Natriuretic peptides Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) Mediates vasodilation and natriuresis Clinical trials with anaritide and nesiritide relatively inconclusive but lower doses and longer infusion times may reduce risk of post-op AKI,53,Glycemic Control,Insulin promising for hospital-acquired ARF prevention Van den Berghe et al randomized patients in a surgical intensive care unit to receive standard control ( 200 mg/dL) or intensive glucose control measures (goal blood glucose concentrations of 80 to 110 mg/dL) tight blood glucose significantly improved mortality 41% reduction in ARF development Reduction in ARF may be consequence of total insulin dose used to treat the patient; possible direct protective effect of insulin,54,55,Treatment for ARF,Treatment,Short-term goals minimize degree of insult to the kidney reduce extrarenal complications expedite renal function recovery Ultimate goal restore renal function to pre-ARF baseline Prerenal hemodynamic support and volume replacement Immune related (interstitial nephritis, glomerulonephritis) promptly initiate immunosuppressive therapy Postrenal remove cause of obstruction,56,Nonpharmacologic,Initial modalities to reverse or minimize prerenal ARF remove medications associated with diminished renal blood flow physically remove prerenal obstruction Dehydration fluid replacement oral rehydration for moderate volume-depleted patients isotonic normal saline IV replacement fluid of choice large volumes may be necessary typically initiated with 250 to 500 mL of normal saline over 15 to 30 minutes with assessment of volume status after each challenge,57,Nonpharmacologic,Patients with ARF on top of preexisting CKD should not be expected to produce urine beyond preexisting baseline Anuria or oliguria initiate slower rehydration (250-mL boluses or 100 mL/h infusions of normal saline) reduces pulmonary edema risk, especially if heart failure or pulmonary insufficiency exists Consider other replacement fluids if dehydration accompanied by severe electrolyte imbalance,58,Nonpharmacologic,Blood loss or symptomatic anemia: transfuse RBCs to hematocrit 30% Albumin sometimes used as a resuscitative agent limit to individuals with severe hypoalbuminemia resistant to crystalloid therapy,59,Nonpharmacologic,Intrinsic or post-obstructive ARF fluid and electrolyte management may become fluid-overloaded due to aggressive fluid resuscitation concentrate drug infusion and nutrition solutions Supportive management 1st line therapy Supportive care goals: maintain adequate cardiac output and BP to allow adequate tissue perfusion