Transcript ACUTE RENAL FAILURE

ACUTE RENAL FAILURE
INTERN EMERGENCY
LECTURE SERIES 2005
DEFINITION
ABRUPT DECREASE IN RENAL
FUNCTION RESULTING IN THE
ACCUMULATION OF
NITROGENOUS COMPOUNDS
SUCH AS UREA AND
CREATININE
A
Acute vs Chronic Renal
Failure
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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
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» Small = Chronic
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Renal Ultrasound
» Increased Echogenicity = Chronic
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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
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PRE-RENAL
55-60%
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POST RENAL
<5%
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RENAL
35-40%
PRE-RENAL ACUTE RENAL
FAILURE
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MOST COMMON CAUSE OF ARF
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RESULTS FROM DECREASED RENAL
PERFUSION
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TREATMENT OF THE CAUSE RESTORES
RENAL FUNCTION TUBULAR FUNCTION
INTACT *
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PROLONGED PRE-RENAL FAILURE MAY
LEAD TO ATN
CAUSES OF PRE-RENAL
AZOTEMIA
Intravascular volume depletion
 Decreased cardiac output
 Systemic vasodilation
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» Antihypertensives
» Sepsis
Renal vasoconstriction
 Drugs impairing autoregulation
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» Ace inhibitors
NSAID
MECHANISMIS OF PRE
RENAL ARF
POST-RENAL ACUTE RENAL
FAILURE
ACCOUNTS FOR 2-15% OF ALL ARF
 OBSTRUCTION TO URINE FLOW
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» INCREASED TUBULAR PRESSURE
» VASOCONSTRICTION
– DECREASED RENAL BLOOD FLOW
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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
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» YOUNG = CONGENITAL ABNORMALITY
» OLDER MALE = PROSTATIC
ENLARGEMENT
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ARF MOST OFTEN ASSOCIATED
WITH LESIONS IN:
» BLADDER, PROSTATE OR URETHRA
RENAL-ACUTE RENAL FAILURE
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VASCULAR DISEASE
» VASCULITIS (SLE, POLYARTERITIS
ETC.)
» SCLERODERMA
» THROMBOEMBOLIC DISEASE
» MALIGNANT HYPERTENSION
RENAL--ACUTE RENAL
FAILURE
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GLOMERULAR DISEASE
» ACUTE GLOMERULONEPHRITIS
–POST INFECTIOUS GN
–CRESCENTIC GN
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ANCA POSITIVE DISEASES
–GOODPASTURE’S DIS.
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ANTI- GLOMERULAR BASEMENT
ANTIBODY
RBC CAST
ACUTE INTERSTITIAL NEPHRITIS
DRUG INDUCED
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PENICILLINS
SULFONAMIDES
CEPHALOSPORIN
RIFAMPIN ( 2ND
TIME)
QUINOLONES
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NSAID
(FENOPROFEN)
ALLOPURINOL
PHENYTOIN
THIAZIDES
FUROSEMIDE
CIMETIDINE
Acute Interstitial Nephritis
 Fever
 Rash
 Eosinophilia
 Pyuria
 Eosinophiluria
 WBC
Casts
WBC Cast
RENAL --ACUTE RENAL FAILURE
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ACUTE TUBULAR NECROSIS
» ISCHEMIC INJURY
» TOXIC INJURY
– ENDOGENOUS TOXINS
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HEMOGLOBINURIA
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MYOBLOBINURIA (RHABDOMYOLYSIS)
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ENDOTOXEMIA
RENAL-- ACUTE RENAL FAILURE
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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
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GEN.MED. --SURG.
INTENSIVE CARE
OPEN HEART SURG
AMINOGLYCOSIDE
BURNS
RHABDOMYOLYSIS
CIS-PLATIN
3-5%
5-25%
5-20%
10-30%
20-60%
20-30%
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
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» 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
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Treatment of Hyperkalemia
Urgency
 Role of the EKG in making the decision
 Clinical setting in which it occurs
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» Acute renal failure
» Chronic renal failure
Table 5-3. Treatment of hyperkalemia
Medication
Mechanism of action
Dosage
Calcium
gluconate
Antagonism of
membrane
Insulin and
Glucose
Increased K+entry
into the cells
Insulin, 10 U IV bolus
followed by 0.5 mU/kg of
body weight per minute in
50 ml of 20% glucose
Sodium
bicarbonate
Increased K+entry
into the cells
44-50 mEq IV over 5 min;
can be repeated within 30
min
Albuterol
Increased K+entry
into the cells
10-30 ml of 10% solution IV
over 2 min
Peak effect
-5 min
30-60 min
30-60 min
20 mg in the nebulized form
30-60 min
Kayexalate
Removal of the
excess K+
20 g of resin with 100 ml of
20% sorbitol; can be
repeated every 4-6 hr
2-4 hr
Hemodialysis
Removal of the
excess K+
Dialysis bath K+ concentration
variable
30-60 min
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,
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METHANOL
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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% *
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CAUSES OF DEATH IN ATN