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INTERN EMERGENCY LECTURE SERIES 2005
ACUTE RENAL FAILURE INTERN EMERGENCY LECTURE SERIES 2005
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ABRUPT DECREASE IN RENAL FUNCTION RESULTING IN THE ACCUMULATION OF NITROGENOUS COMPOUNDS SUCH AS UREA AND CREATININE DEFINITION
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A
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Acute vs Chronic Renal Failure
History Known Chronic Recent Toxic Exposure Recent Hypoxic Insult Recent Trauma Known Diseases Associated with ARF Prev. Abnormal Lab Results Suggesting Chronic History of normal renal function 4 months previously suggests acute History of normal BP one year ago suggests new onset hypertension
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Acute vs Chronic Renal Failure
Rapidly Rising Creatinine = Acute Kidney Size Small = Chronic Renal Ultrasound Increased Echogenicity = Chronic Urine Flow Rate Oliguric or Anuric usually = Acute Normal kidney size suggests acute echogenicity only mildly increased suggests acute oligoanuria suggests acute
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ACUTE RENAL FAILURE CLASSIFICATION BY URINE VOLUME
OLIGURIC: <400 CC/ 24 Hrs NON-OLIGURIC: >500 CC/24 Hrs ANURIC <50 CC/24 Hrs
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ETIOLOGY OF ACUTE RENAL FAILURE
PRE-RENAL % POST RENAL <5% RENAL %
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PRE-RENAL ACUTE RENAL FAILURE
MOST COMMON CAUSE OF ARF RESULTS FROM DECREASED RENAL PERFUSION TREATMENT OF THE CAUSE RESTORES RENAL FUNCTION TUBULAR FUNCTION INTACT * PROLONGED PRE-RENAL FAILURE MAY LEAD TO ATN
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CAUSES OF PRE-RENAL AZOTEMIA
Intravascular volume depletion Decreased cardiac output Systemic vasodilation Antihypertensives Sepsis Renal vasoconstriction Drugs impairing autoregulation Ace inhibitors NSAID
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MECHANISMIS OF PRE RENAL ARF
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POST-RENAL ACUTE RENAL FAILURE
ACCOUNTS FOR 2-15% OF ALL ARF OBSTRUCTION TO URINE FLOW INCREASED TUBULAR PRESSURE VASOCONSTRICTION DECREASED RENAL BLOOD FLOW MUST BE BILATERAL TO RESULT IN ARF UNLESS : SINGLE KIDNEY OR PRIOR CHRONIC RENAL FAILURE
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POST RENAL ACUTE RENAL FAILURE
SUSPECT OBSTRUCTION IN ANURIA ETIOLOGY MAY BE AGE DEPENDENT YOUNG = CONGENITAL ABNORMALITY OLDER MALE = PROSTATIC ENLARGEMENT ARF MOST OFTEN ASSOCIATED WITH LESIONS IN: BLADDER, PROSTATE OR URETHRA
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RENAL-ACUTE RENAL FAILURE
VASCULAR DISEASE VASCULITIS (SLE, POLYARTERITIS ETC.) SCLERODERMA THROMBOEMBOLIC DISEASE MALIGNANT HYPERTENSION
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RENAL--ACUTE RENAL FAILURE
GLOMERULAR DISEASE ACUTE GLOMERULONEPHRITIS POST INFECTIOUS GN CRESCENTIC GN ANCA POSITIVE DISEASES GOODPASTURE’S DIS. ANTI- GLOMERULAR BASEMENT ANTIBODY
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RBC CAST
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ACUTE INTERSTITIAL NEPHRITIS DRUG INDUCED
PENICILLINS SULFONAMIDES CEPHALOSPORIN RIFAMPIN ( 2ND TIME) QUINOLONES NSAID (FENOPROFEN) ALLOPURINOL PHENYTOIN THIAZIDES FUROSEMIDE CIMETIDINE
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Acute Interstitial Nephritis
Fever Rash Eosinophilia Pyuria Eosinophiluria WBC Casts
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WBC Cast
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RENAL --ACUTE RENAL FAILURE
ACUTE TUBULAR NECROSIS ISCHEMIC INJURY TOXIC INJURY ENDOGENOUS TOXINS HEMOGLOBINURIA MYOBLOBINURIA (RHABDOMYOLYSIS) ENDOTOXEMIA
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RENAL-- ACUTE RENAL FAILURE
ACUTE TUBULAR NECROSIS EXOGENOUS TOXINS AMINOGLYCOSIDES RADIOGRAPHIC CONTRAST HEAVY METAL COMPOUNDS ETHYLENE GLYCOL METHANOL CARBON TETRACHLORIDE CIS PLATIN
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HIGH RISK SETTINGS FOR ATN
CLINICAL SETTING FREQUENCY GEN.MED. --SURG % INTENSIVE CARE % OPEN HEART SURG 5-20% AMINOGLYCOSIDE % BURNS % RHABDOMYOLYSIS % CIS-PLATIN %
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ATN SEDIMENT
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DIAGNOSTIC APPROACH TO ARF
HISTORY PHYSICAL EXAMINATION ASSMENT OF URINE VOLUME URINE ANALYSIS BLOOD CHEMISTRY BLOOD AND URINE INDICES RADIOLOGIC STUDIES
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Treatment of ARF
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Hyperkalemia Never occurs in the absence of renal excretory problem
Pseudohyperkalemia Leukocytosis Thrombocytosis Prolonged Application of Tourniquet
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Hyperkalemia Significance of urine output
Role of increased catabolism or tissue breakdown Factors affecting shift of Potassium out of cells Etiololgy of the renal failure
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Treatment of Hyperkalemia
Urgency Role of the EKG in making the decision Clinical setting in which it occurs Acute renal failure Chronic renal failure
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Table 5-3. Treatment of hyperkalemia
Medication Mechanism of action Dosage Peak effect Calcium Antagonism of ml of 10% solution IV min gluconate membrane over 2 min Insulin and Increased K+entry Insulin, 10 U IV bolus min Glucose into the cells followed by 0.5 mU/kg of body weight per minute in 50 ml of 20% glucose Sodium Increased K+entry mEq IV over 5 min; min bicarbonate into the cells can be repeated within 30 min Albuterol Increased K+entry into the cells mg in the nebulized form min Kayexalate Removal of the g of resin with 100 ml of hr excess K % sorbitol; can be repeated every 4-6 hr Hemodialysis Removal of the Dialysis bath K+ concentration min excess K variable
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INDICATIONS FOR DIALYSIS IN ACUTE RENAL FAILURE
UREMIC SYMPTOMS ~ nausea ~ neurologic SEVERE FLUID OVERLOAD REFRACTORY ELECTROLYTE DISORDERS ~hyperkalemia SEVERE REFRACTORY ACIDOSIS
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INDICATIONS FOR DIALYSIS IN ACUTE RENAL FAILURE
PERICARDITIS NEUROPATHY MENTAL STATUS CHANGE SEIZURES BLEEDING TOXINS----ETHYLENE GLYCOL, METHANOL PROPHYLACTIC ~recent studies fail to document benefit
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MORTALITY ASSOCIATED WITH SETTING OF ATN
OVERALL MORTALITY % POST TRAUMATIC % MEDICAL CAUSE % SURGICAL CAUSE % NON-OLIGURIC 26% * OLIGURIC 50% *
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CAUSES OF DEATH IN ATN
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