13 Evaluation And Management Of Acute Renal Failure
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13 Evaluation And Management Of Acute Renal Failure

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13 Evaluation And Management Of Acute Renal Failure 13 Evaluation And Management Of Acute Renal Failure Presentation Transcript

  • Evaluation and Management of Acute Renal Failure 范揚智醫師 95/10/12
  • 腎臟的功能 調節水份 調節酸鹼 調節電解質 尿液的形成 內分泌器官– Vitamin D, erythropoietin, RAS
    • Anuria: urine < 100ml/day
    • Oliguria: urine <400-500 mL/d
    • Azotemia: Increase Cr, BUN
    • May be prerenal, renal, postrenal
    • Does not require any clinical findings
    • Chronic Kidney Disease: graduated loss of renal function, National kidney fundation: stage 1~5
    • ESRD = Loss of kidney function >3 months
    View slide
  • Blood Urea Nitrogen (BUN)
    • Catabolism of aminoacids generates NH 3
            • NH 2
        • 2 NH 3 + CO 2 = C = 0 + H 2 O
            • NH 2
    • Urea Mol wt : 60; BUN Mol wt. : 28
    • Normal BUN 10-20 mg/dl
    • After filtration › 50% is reabsorbed by the tubule
    • BUN level is related to: Renal function, protein intake, liver function, GI bleeding, steroid, hyper catabolic states
    View slide
  • Creatinine
    • Formed at a constant rate by dehydration of muscle creatine
    • Normally 1–2% of muscle creatine is broken into creatinine
    • Mol. Wt. 113
    • Creatinine is freely filtered by the glomerulii and is not reabsorbed 10–15% is secreted into proximal tubule
  • GFR Estimation by Plasma Creatinine
      • Cockcroft and Gault Formula*
      • Calculated creatinine clearance
      • = (140–age) x wt (kg)
      • 72 X serum creatinine(mg/dl)
      • For females, subtract 15% (or multiply by 0.85); for paraplegics multiply by 0.8, for quadriplegics, multiply by 0.6
      • *Applicable only when patient is in a steady state, not edematous and not obese
  • Factors that affect serum creatinine concentration Positive interference with picric acid assay for creatinine Increase Ketoacidosis Inhibition of tubular creatinine secretion Increase Use of cimetidine, trimethoprim Transient increase in creatinine generation (increase may be blunted by transient increase in GFR) Increase Ingestion of cooked meat Reduced creatinine generation (common in children, women, and older and malnourished patients) Decrease Reduced muscle mass Decreased GFR(increase is blunted by increased tubular secretion of creatinine and by reduced creatinine generation) Increase Kidney Disease Mechanism (comment) Effect on serum creatinine Factor
  • Acute Renal Failure
    • Definition:
    • Rapid (hours to weeks) decline in glomerular filtration rate and retention of waste products
    • It is a clinical syndrome cause by many renal or extrarenal diseases
    • Lack a uniform definition
      • Cr > 1.5x, urine output <0.5ml/kg/hr
      • Cr increase ≥ 1.0 mg/dl/2d
  • The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group
  • The facts you need to know about ARF
    • Acute renal failure may reversible and should look for the causes to management
    • Incidence:
    • - 2-5% of hospitalized patients(55% iatrogenic)
    • - 7-23% of ICU patients
    • - 20-60% require dialysis; of those who survive initial dialysis, <25% require long-term dialysis
  • The facts you need to know about ARF
    • Motality:
      • Liano(1996) reported mortality rate of 60% for patient with ATN, 35% for acute on chronic renal failure, 27% for obstructive ARF and 26% for renal disorder other than ATN.
      • Knaus(1986)50% for combination of acute renal and respiratory failure towards 100% with 5 system failure
      • In community-acquired ARF with mostly prerenal and postrenal causes and the prognosis is better.
      • Rates not significantly decreased over past 50 years despite advances in dialysis and critical care (increased patient age and co morbid illnesses)
  • Symptoms and Signs of Renal Failure
    • Retention of nitrogenous waste products
      • Nausea, vomiting, diarrhea, hiccup, foul taste, dry crusted mouth, itching,
      • Drowsiness, clouding of consciousness, neuropathy, pericarditis, GI bleeding,
      • Coma
    • Retention of salt and water
      • Pulmonary edema, peripheral edema, ascites, pleural effusion
  • Symptoms and Signs of Renal Failure
    • Retention of potassium
      • Weakness, lassitude, paralysis, EKG changes with tenting T waves, widening of QRS complex, increased PR interval, sine wave pattern, cardiac arrest, VT
    • Retention of acid
      • Kussmaul respiration, hyperreflexia, hypotension
  • A: Cr, BUN B: H, P, K C: NaCl
  • Classification of ARF Acute Renal Failure Pre-renal Intrinsic Post-renal Glomerular Interstitial Vascular Tubular
  • Pre-renal ARF
    • Accounts for 60-70% of cases of ARF
    • Represents physiologic response to mild-moderate renal hypoperfusion
    • Renal parenchymal tissue is not damaged therefore rapidly reversible upon restoration of RBF and glomerular filtration pressure
    • Elderly and those with pre-existing renal disease at increased risk
  • Pre-renal ARF
    • I. Hypovolemia
    • A. Hemorrhage, burns, dehydration
    • B. GI fluid loss: vomiting, surgical drainage, diarrhea
    • C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypoadrenalism
    • D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns, severe hypoalbuminemia
    • II. Low cardiac output
    • A. Diseases of myocardium, valves, and pericardium; arrhythmias; tamponade
    • B. Other: pulmonary hypertension, massive pulmonary embolus, positive pressure mechanical ventilation
  • Pre-renal ARF
    • III. Altered renal systemic vascular resistance ratio
    • A. Systemic vasodilatation: sepsis, antihypertensives, afterload reducers, anesthesia, anaphylaxis
    • B. Renal vasoconstriction: hypercalcemia, norepinephrine, epinephrine, cyclosporine, tacrolimus, amphotericin B
    • C. Cirrhosis with ascites (hepatorenal syndrome)
    • IV. Renal hypoperfusion with impairment of renal autoregulatory responses
    • Cyclooxygenase inhibitors, ACEI
    • V. Hyperviscosity syndrome (rare)
    • Multiple myeloma, macroglobulinemia, polycythemia
  • Intrinsic Renal Causes
    • Accounts for 25-40% of cases of ARF
    • Types:
      • Acute glomerulonephritis <5%
      • Interstitial nephritis 10%
      • Intrarenal vascular disease <5%
      • ATN 85%
    • I. Renovascular obstruction (bilateral or unilateral in the setting of one functioning kidney)
    • A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissecting aneurysm, vasculitis
    • B. Renal vein obstruction: thrombosis, compression
    • II. Disease of glomeruli or renal microvasculature
    • A. Glomerulonephritis and vasculitis
    • B. Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, toxemia of pregnancy, accelerated hypertension, radiation nephritis, systemic lupus erythematosus, scleroderma
    Intrinsic Renal Causes
  • Intrinsic Renal Causes
    • III. Acute tubular necrosis
    • A. Ischemia(60%): as for prerenal ARF (hypovolemia, low cardiac output, renal vasoconstriction, systemic vasodilatation), obstetric complications (abruptio placentae, postpartum hemorrhage)
    • B. Toxins(40%)
    • 1. Exogenous: radiocontrast, cyclosporine, antibiotics (e.g., aminoglycosides), chemotherapy (e.g., cisplatin), organic solvents (e.g., ethylene glycol), acetaminophen, illegal abortifacients
    • 2. Endogenous: rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (e.g., myeloma)
  • Intrinsic Renal Causes
    • IV. Interstitial nephritis
    • A. Allergic: antibiotics (e.g., -lactams, sulfonamides, trimethoprim, rifampicin), nonsteroidal anti-inflammatory agents, diuretics, captopril
    • B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral (e.g., cytomegalovirus), fungal (e.g., candidiasis)
    • C. Infiltration: lymphoma, leukemia, sarcoidosis
    • D. Idiopathic
    • V. Intratubular deposition and obstruction
    • Myeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulphonamides
    • VI. Renal allograft rejection
  • Post-renal Causes of ARF
    • Account for 5% of cases of ARF
    • ARF occurs when both urinary outflow tracts are obstructed or when one tract is obstructed in a patient with a single functional kidney
  • Post-renal Causes of ARF
    • I. Ureteric
    • Calculi, blood clot, sloughed papillae, cancer, external compression (e.g., retroperitoneal fibrosis)
    • II. Bladder neck
    • Neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot
    • III. Urethra
    • Stricture, congenital valve, phimosis
  • Investigations
    • ARF: Focused History
    • Nausea? Vomiting? Diarrhea?
    • Hx of heart disease, liver disease, previous renal disease, kidney stones, BPH?
    • Any recent illnesses?
    • Any edema, change in
    • urination?
    • Any new medications?
    • Any recent radiology studies?
    • Rashes?
  • Investigations
    • Physical Examination:
    • Infection sign ? Blood pressure, vital sign
    • Volume Status
      • Mucus membranes, orthostatics, skin turgor, Edema
    • Cardiovascular
      • JVD, rubs
    • Pulmonary
      • Decreased breath sounds
      • Rales
    • Abd and back: bladder distension, masses, ascites, CVA tenderness, large prostate
    • Rash (Allergic interstitial nephritis)
  • Investigations
    • Blood
      • CBC-DC
      • Electrolyte, Ca, Mg, P
      • Urea, Creatinine
      • Others: LDH, Alb, CRP…
    • Urine
      • Urine sodium, Cr
      • Urine osmolality
      • Urinalysis
    • Renal echo
  •  
  • FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr)
    • FeNa <1%
    • 1. PRERENAL
    • Urine Na < 20. Functioning tubules reabsorb lots of filtered Na
    • 2. ATN (unusual)
    • Postischemic dz: most of UOP comes from few normal nephrons, which handle Na appropriately
    • ATN + chronic prerenal dz (cirrhosis, CHF)
    • 3. Glomerular or vascular injury
    • Despite glomerular or vascular injury, pt may still have well-preserved tubular function and be able to concentrate Na
  • More FeNa
    • FeNa 1%-2%
    • Prerenal-sometimes
    • ATN-sometimes
    • AIN-higher FeNa due to tubular damage
    • FeNa >2%
    • ATN Damaged tubules can't reabsorb Na
    • Calculating FeNa after pt has gotten Lasix.
    • 1. Fractional Excretion of Lithium (endogenous) (<7% in prerenal )
    • 2. Fractional Excretion of Uric Acid (<7% in prerenal )
  •  
  • I s the renal failure really acute?
    • Factors suggesting chronicity
    • Duration of symptoms for months
    • Absence of acute illness in the face of very high urea and creatinine
    • Anaemia of chronic disorders
    • Bone disease (renal osteodystrophy)
    • Sexual dysfunction
    • Skin disorders, pruritus
    • Neurological complications
    • Small kidneys on renal imaging
  • Management
    •    Prevention
    •    Etiology treatment
    •    Prevention additional injury
    •    Treatment of complication
    •    Conservative measurement
    •    Renal replacement therapy
  • Prevention
    • Identification of high-risk patients for pharmacologic agents-induced nephrotoxicity
      • iodinated radiocontrast medium, NSAIDs
    • Aggressive surveillance for nephrotoxin-induced renal dysfunction
      • cisplatin, amphotericin B, aminoglycoside
    • Use of volume expansion in selected clinical settings
      • Hyperpigmenturia: hemoglobinuria, myoglobinuria
      • Crystaluria: uric acid, acyclovir, methotrexate, sulfonamides
    • Minimalization of catheters use to avoid nosocomial sepsis
  • Etiology Treatment
    • Correct postrenal factor
    • Correct prerenal factor
    • Treat underlying sepsis
    • Stop nephrotoxic drugs
  • Conservative Measurement
    • Fluid balance
      • Careful monitoring of I/O and body weight
    • Fluid restriction
      • (usually less than 1 L/day in oliguric ARF)
      • Total intake < urine output +extrarenal losses
    • Electrolytes and acid -base balance
      • hyperkalemia
      • hyponatremia
      • Keep serum bicarbonate >15
      • hyperphosphatemia
      • Treat hypocalcemia only if symptomatic
  • Guide of Volume Expansion
    • CVP 8-14 cm H 2 O (5-2 rule)
    • PAWP 12-16 mmHg (7-3 rule)
    • Urine output 0.5-1.0ml/kg/hour
    • Weighing the patient daily
    • Insensible water loss from the skin and respiratory tract (500 ml/day)
  • Dietary modification
    • total caloric intake– 35~ 50 kcal/kg/day
    • to avoid catabolism
    • Salt restriction– 2~4 g/day
    • Potassium intake– 40 meq/day
    • Phosphorus intake– 800 mg/day
    • Uremia-nutrition
      • Restriction protein is not necessary in ARF, maintain caloric intake
      • Carbohydrate ≥ 100gm/day to minimize ketosis and protein catabolism
    • Drug
      • Review all medication, Stop magnesium-containing medication
      • Adjusted dosage for renal failure, Readjust with improvement of GFR
    Conservative Measurement
  • Indication of Dialysis
    • Absolute indication
    • CCr  5 ml/min or serum Cr  10.0 mg/dl
    • Relative indication
    • CCr  10 ml/min or serum Cr  8.0 mg/dl
    • With accompanied symptoms or signs
    • = CHF/Pulmonary edema = Uremic pericarditis = Bleeding tendency = Neurologic symptoms = Drug-resistant hyper-K = Drug-resistant metabolic acidosis = Drug-resistant nausea/vomiting = Others
  • Take Home Points
    • Features of the history and physical examination in addition to relevant lab and radiologic investigations help to determine the most likely cause(s) of ARF in a given patient
  • Take Home Points
    • Management of a patient with ARF involves:
      • Treating potentially life-threatening complications
      • Reversing pre-renal and post-renal causes
      • Minimizing further hemodynamic and toxic insults to the kidney
      • Admission and appropriate consultation
      • Lack of evidence for converting oliguric to non-oliguric ARF