ACUTE RENAL FAILURE 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

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

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 NEPHRITISDRUG INDUCED

PENICILLINS SULFONAMIDES CEPHALOSPORIN RIFAMPIN ( 2ND

TIME) QUINOLONES

NSAID (FENOPROFEN)

ALLOPURINOL PHENYTOIN THIAZIDES FUROSEMIDE CIMETIDINE

FeverRashEosinophiliaPyuriaEosinophiluriaWBC Casts

Acute Interstitial Nephritis

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

minAlbuterol 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