INTERN EMERGENCY LECTURE SERIES 2005 ACUTE RENAL FAILURE INTERN EMERGENCY LECTURE SERIES 2005
ABRUPT DECREASE IN RENAL FUNCTION RESULTING IN THE ACCUMULATION OF NITROGENOUS COMPOUNDS SUCH AS UREA AND CREATININE DEFINITION
A
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
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
ACUTE RENAL FAILURE CLASSIFICATION BY URINE VOLUME OLIGURIC: <400 CC/ 24 Hrs NON-OLIGURIC: >500 CC/24 Hrs ANURIC <50 CC/24 Hrs
ETIOLOGY OF ACUTE RENAL FAILURE PRE-RENAL 55-60% POST RENAL <5% RENAL 35-40%
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
CAUSES OF PRE-RENAL AZOTEMIA Intravascular volume depletion Decreased cardiac output Systemic vasodilation Antihypertensives Sepsis Renal vasoconstriction Drugs impairing autoregulation Ace inhibitors NSAID
MECHANISMIS OF PRE RENAL ARF
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
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
RENAL-ACUTE RENAL FAILURE VASCULAR DISEASE VASCULITIS (SLE, POLYARTERITIS ETC.) SCLERODERMA THROMBOEMBOLIC DISEASE MALIGNANT HYPERTENSION
RENAL--ACUTE RENAL FAILURE GLOMERULAR DISEASE ACUTE GLOMERULONEPHRITIS POST INFECTIOUS GN CRESCENTIC GN ANCA POSITIVE DISEASES GOODPASTURE’S DIS. ANTI- GLOMERULAR BASEMENT ANTIBODY
RBC CAST
ACUTE INTERSTITIAL NEPHRITIS DRUG INDUCED PENICILLINS SULFONAMIDES CEPHALOSPORIN RIFAMPIN ( 2ND TIME) QUINOLONES NSAID (FENOPROFEN) ALLOPURINOL PHENYTOIN THIAZIDES FUROSEMIDE CIMETIDINE
Acute Interstitial Nephritis Fever Rash Eosinophilia Pyuria Eosinophiluria WBC Casts
WBC Cast
RENAL --ACUTE RENAL FAILURE ACUTE TUBULAR NECROSIS ISCHEMIC INJURY TOXIC INJURY ENDOGENOUS TOXINS HEMOGLOBINURIA MYOBLOBINURIA (RHABDOMYOLYSIS) ENDOTOXEMIA
RENAL-- ACUTE RENAL FAILURE ACUTE TUBULAR NECROSIS EXOGENOUS TOXINS AMINOGLYCOSIDES RADIOGRAPHIC CONTRAST HEAVY METAL COMPOUNDS ETHYLENE GLYCOL METHANOL CARBON TETRACHLORIDE CIS PLATIN
HIGH RISK SETTINGS FOR ATN CLINICAL SETTING FREQUENCY GEN.MED. --SURG. 3-5% INTENSIVE CARE 5-25% OPEN HEART SURG 5-20% AMINOGLYCOSIDE 10-30% BURNS 20-60% RHABDOMYOLYSIS 20-30% CIS-PLATIN 15-25%
ATN SEDIMENT
DIAGNOSTIC APPROACH TO ARF HISTORY PHYSICAL EXAMINATION ASSMENT OF URINE VOLUME URINE ANALYSIS BLOOD CHEMISTRY BLOOD AND URINE INDICES RADIOLOGIC STUDIES
Treatment of ARF
Hyperkalemia Never occurs in the absence of renal excretory problem Pseudohyperkalemia Leukocytosis Thrombocytosis Prolonged Application of Tourniquet
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
Treatment of Hyperkalemia Urgency Role of the EKG in making the decision Clinical setting in which it occurs Acute renal failure Chronic renal failure
Table 5-3. Treatment of hyperkalemia Medication Mechanism of action Dosage Peak effect Calcium Antagonism of 10-30 ml of 10% solution IV -5 min gluconate membrane over 2 min Insulin and Increased K+entry Insulin, 10 U IV bolus 30-60 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 44-50 mEq IV over 5 min; 30-60 min bicarbonate into the cells can be repeated within 30 min Albuterol Increased K+entry into the cells 20 mg in the nebulized form 30-60 min Kayexalate Removal of the 20 g of resin with 100 ml of 2-4 hr excess K+ 20% sorbitol; can be repeated every 4-6 hr Hemodialysis Removal of the Dialysis bath K+ concentration 30-60 min excess K+ variable
INDICATIONS FOR DIALYSIS IN ACUTE RENAL FAILURE UREMIC SYMPTOMS ~ nausea ~ neurologic SEVERE FLUID OVERLOAD REFRACTORY ELECTROLYTE DISORDERS ~hyperkalemia SEVERE REFRACTORY ACIDOSIS
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
MORTALITY ASSOCIATED WITH SETTING OF ATN OVERALL MORTALITY 40-60% POST TRAUMATIC 70-90% MEDICAL CAUSE 15-40% SURGICAL CAUSE 40-80% NON-OLIGURIC 26% * OLIGURIC 50% *
CAUSES OF DEATH IN ATN