【持续性肾脏替代治疗crrt英文精品课件】acute kidney injury(91p)

Acute Kidney Injury,N. Ganesh Yadlapalli, M.D. Assistant Professor of Medicine University of Cincinnati,Overview of AKI,Definition of AKI Pathophysiology Pre-renal Renal: glomerular, tubular, interstitial and vascular. Post renal: obstruction. Clinical features Investigations Treatment Prevention,AKI Definition,Sudden rapid drop in GFR, as measured by serum creatinine level, over hours to days.,AKI: An abrupt increase in serum creatinine of at least 0.3 mg/dl or 1.5 fold of baseline within 48 hours. Stage I: Increase in Creatinine 1.5 to 2 fold Stage II: Increase in Creatinine 2.0 to 3 fold Stage III: Increase in Creatinine 3.0 times or Dialysis requirement (or a peak creatinine of 4.0 mg/dl with at least a 0.5 mg/dl increase),Diagnostic Criteria for AKI,Acute Kidney Injury Network Consensus Statement, 2007,AKI Serum Creatinine,Pathophysiology,Pathophysiology,AKI: Pathophysiology,Reasons for AKI Consults (n = 748),Pre-renal 21% Renal ATN 45% ARF or CRI 13% GN 4% AIN 2% AED 1% Obstruction 10%,Liano et al. Kidney Int 1996;50:811.,AKI: Prerenal,Prerenal,“True” Volume depletion - Blood loss - GI or Renal losses Intravascular Volume Depletion Effective circulating volume depletion - Congestive heart failure - Cirrhosis - Nephrosis - Sepsis/vasodilated states,History Dry mucosa, skin turgor Hypotension Oliguria,History Edematous states,Blood Volume Cardiac Pump dysfunction Vasodilation Glomerular autoregulation,AKI: Intra Renal,Glomerular Vascular Tubules Interstitial,Intra Renal- Glomerular Disease,Pathology: Focal and diffuse glomerulonephritis Cresentic GN Hallmark: Red blood cell casts Hematuria, HTN,Intra Renal - Vascular Disease,Common causes: Malignant HTN Vasculitis Thromboembolic disease,Intra Renal -Acute Tubular Necrosis,85% - intrinsic AKI Histologic changes Epithelial sloughing Luminal occlusion Common causes Ischemia Toxic Rhabdomyolysis/myoglobinuria,AKI: Tubules,ATN a) Neprotoxic agents Drugs: Amphotercin, aminoglycosides Myoglobin, hemoglobin, radio-contrast b) Ischemic injury Prolonged prerenal state, Shock Arterial cross clamping during AAA and CABG Afferent arteriolar constriction sec to severe hypercalcemia. Tubular obstruction a) Crystal induced tubular obstructions Allopurinol, sulpha, HIV meds, methotrexate,AKI: Acute Interstitial Nephritis,10% - intrinsic ARF Classic presentation Fever, rash, eosinophilia Eosinophiluria Definitive Dx = renal biopsy,AKI: Interstitial Nephritis,AKI: Interstitial Nephritis,AKI: Post Renal,Anuria - important finding Common causes of obstruction Prostatic obstruction Cancer Retroperitoneal disease Dx = ultrasound,Post Renal AKI,Ureteral and pelvic Intrinsic obstruction Blood clots Stones/crystals Sloughed papillae Fungus balls Extrinisic obstruction Malignancy Retroperitoneal fibrosis Iatrogenic: inadvertent ligation,Bladder Stones Blood clots Prostatic hypertrophy or malignancy Bladder carcinoma Neuropathic Urethral Strictures Phimosis,Clinical Features,AKI: Clinical Features,Common symptom is oliguria (400ml/d). anuria (50ml/d) is uncommon. Anuria is uncommon and if present, suspect Arterial thrombosis, venous thrombosis, Cortical necrosis, severe ATN, Complete obstruction,AKI: Clinical features,Clinical features of underlying disease: Pre renal state: patients have symptoms and signs of hypovolemia. Rhabdomyolysis: history of crush injury, hyperthermia, prolonged seizures, muscle damage after lay down in the same position for prolonged period secondary to alcohol intoxication, stroke, drugs. Interstitial nephritis: Classic presentation is combination of fever, rash, arthalgias eosinophilia and eosinophiluria. Signs and symptoms of uremia in patients with severe renal failure.,Clinical Assessment,Progression of ATN,Death 50%,Acute Renal Failure,15% Complete Recovery,30% Incomplete Recovery,5% No Recovery,25% Function Stable,5% Function Regresses,Oliguric vs. Nonliguric AKI*,Severity Maximum BUN (mg/100 ml) 114 95 Maximum SCr (mg/100 ml) 9 6 Hospitalization (days) 31 22 Required dialysis (%) 84 28 Morbidity (%) Gastrointestinal bleeding 39 19 Septic episode 42 20 Metabolic acidosis 45 20 Neurologic abnormality 50 30 Mortality 50 20,*All differences were statistically significant,Oliguric,Non-Oliguric,Workup,AKI: Workup,Basic investigations Renal panel and CBC Foley (to relieve obstruction and measure PVR) UA and culture Urine electrolytes (Na and creatinine) Renal ultrasound,AKI: Other Tests,Renal blood-flow scan Gallium scan CT scan Renal angiography Renal biopsy,Clinical Utility of Urinalysis,A 52-year-old male with hypertension, atherosclerotic PVD and a baseline SCr of 1.5 mg/dL is admitted for CABG. Post-op course is complicated by two episodes of hypotension, painful bluish lesions on three toe tips, and pneumonia treated with penicillin. Six days post-op his SCr is 5.4 mg/dL.,Question 1,The ARF could be due to: A. Acute tubular necrosis B. Acute interstitial nephritis C. Bladder outlet obstruction D. Atheroembolic renal disease E. All of the above,If urinalysis showed: Dipstick: protein 1+ blood 2+ Sediment: Many WBCs, RBCs Hansels stain positive for eosinophils,Question 2,Question 2,ARF would most likely be due to: A. Acute tubular necrosis B. Acute interstitial nephritis C. Bladder outlet obstruction D. Atheroembolic renal disease E. All of the above,If urinalysis showed: Dipstick: protein trace blood negative Sediment: Many dirty brown casts,Question 3,Question 3,The ARF would most likely be due to: A. Acute tubular necrosis B. Acute interstitial nephritis C. Bladder outlet obstruction D. Atheroembolic renal disease E. All of the above,Copyright 2004 American Society for Clinical Investigation,Schrier, R. W. et al. J. Clin. Invest. 2004;114:5-14,FeNA Vs FeUrea,FeNA 1 Specificity 80% Sensitivity 50% with diuretics FeUrea Sensitivity 88% (with or without diuretics),(Carvounis et al, Kidney Int, Dec 2002),FeNa in AKI,Low FeNa Typicaly seen in prerenal conditions Other causes Hepatorenal syndrome Acute GN ATN sec to contrast, rhabdomyolysis,High FeNA in prerenal AKI If the patient is on diuretic treatment,Treatment,AKI Treatment,Look for reversible causes of AKI Pre-renal conditions (hypovolemia) IV fluids- Normal Saline Delay in IV fluids can lead to prolonged ischemia and tubular damage (ATN) Obstruction Foley catheter,AKI: Treatment,IV fluids First step is to hydrate the patient. Normal saline is preferable Watch vital signs and urine out put IV fluids should be given until vital signs are stable. Back off on fluid resuscitation: If there is no improvement in the urine out, or signs of fluid overload.,AKI: Treatment,Foley catheter: To diagnose and treat obstruction. Asses post void residual volume.,AKI: Treatment,Diuretics In oliguria ARF If oliguria persists after fluid resuscitation Diuretics may convert oliguric to non-oliguric AKI. This may prevent patient going into fluid overload status. In general loop diuretics are preferable in patients with lower GFR.,Oliguric to Nonoliguric,Furosemide: IV bolus of 60-120 mg and escalate the dose if there is no response. It can be given 3-4 times, q 4-6 hours based on clinical response. Or Infusion: 10-40 mg/hour as continuous IV infusion Torsemide IV bolus of 20-40 mg over 5-10 min, and double the dose for appropriate response up to a max dose of 200 mg/day Or Bumetanide IV bolus of 1-2 mg over 1-20 min, and double the dose if no response in 1-2 h to total max 10 mg/day. And Metolazone 5-10 mg PO (max 20 mg/24h) 30 min before a loop diuretic.,Low dose Dopamine in Early AKI,328 patients randomly assigned to low-dose dopamine infusion in ICU Primary endpoint Peak SCr during infusion No difference in Peak creatinine Dialysis requirement ICU/Hospital stay Mortality,Bellomo R et al; Lancet 2000; 356: 2139-43,“Low Dose” Dopamine,Bellomo et al, Lancet 356(9248); Dec 2000,Renal Replacement Therapy,Modalities of RRT in AKI,Intermittent: HD Peritoneal,Continuous: CRRT Ultrafiltration( SCUF) Hemofiltration( CAVH, CVVH) Hemodialysis( CAVHD, CVVHD) Hemodiafiltration( CVVHDf),Nomenclature,RRT in AKI,Timing Type Treatment dose,Initial Choice of RRT for AKI,IHD Hemodynamically stable Severe hyperkalemia CRRT Hemodynamically unstable Can not tolerate fluid removal Intracranial bleed PD,PD Vs CRRT,PD,IPD, CAPD, CCPD,CFPD Common modality in pediatric patients Limitations: - Effect on respiratory status - ? in using it in abdominal sepsis or abdominal surgery - Relative inefficiency in removing waste products in a catabolic patient -High incidence of associated peritonitis,PD vs CRRT,Patients with severe falciparum malaria (48 patients) and sepsis (22 patients) Assignment: 34 to hemofiltration and 36 to PD. PD: 70 liters/ day of dialyzate was used CVVH: 25 liters of replacement fluid was used Replacement fluid was lactate based with glucose of 2g/L Dialyzate was Acetate based with glucose of 15g/L Results: PD has Lower rate of resolution of acidosis Slower rate of decline in plasma Creatinine Markedly increased risk of death,IHD Vs CRRT,IHD,Common mode of treatment of ARF Questions IHD Vs CRRT Daily or every other day Precautions: Patients with cardiovascular instability,CRRT Dose,High Vs Low clearance,CRRT Dose: High Vs Low clearance,VA NIH ARF trail network, NEJM, V 359, no 1, July 2008.,IHD Dose,Daily Vs Alternate day IHD,Schiffl H, N Engl J Med 2002;346:305-310,Daily Vs Alternate day IHD,Schiffl H, N Engl J Med 2002;346:305-310,Timing of Dialysis,Timing of Initiation of Dialysis,Chertow et al, CJASN, 07,Summary of CRRT Type of RRT: CRRT in critically ill and hemodynamically unstable patients Initiation of RRT: Earlier the better Dose and quality: More better and convection clearance For non renal causes : Should be considered, ex. Toxins Special cases: Patients with sepsis, MODS or multiple trauma, role of RRT is to support rather than replace renal function,Advantages of CRRT,Suitable for use in hemodynamically unstable patients Precise volume control Very effective control of uremia Nurses with minimal training can take care of it Safer in patients with brain injuries and cardiovascular disorders. Probable advantages in terms of renal recovery,Disadvantages of CRRT,Expensive compared to IHD Anticoagulation to prevent extra corporeal circuit from Clotting Complications of line insertion and sepsis.,Prevention of AKI,Prevention of Contrast induced AKI,For studies where iodinated contrast material is used (for CT scan, angiography). Hydration is main mode of treatment: Isotonic Na bicarbonate: A bolus of 3 mL/kg for one hour prior to the procedure and continued at a rate of 1 mL/kg/hour for six hours after the procedure. (Add 150 mEq of Na bicarbonate to 850 ml of D5W to prepare Na bicarbonate solution. Or Isotonic saline: At a rate of 1 mL/kg/hour, begun 12 hours prior to the procedure, and continuing for 12 hours after contrast administration. N acetylcysteine: 600 to 1200 mg orally, twice daily on the day before and day of procedure. There is no role for mannitol, diuretics or prophylactic dialysis.,Pigment-induced AKI,Consider prophylaxis: If CK levels 5,000 U/L, In severe crush