Download Acute Renal Failure

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Acute Renal Failure
Internal Medicine Lecture Series
August 10, 2005
Julia Faller, D.O.
Objectives
 Define acute renal failure (ARF)
 Describe the pathophysiology of ARF
 Outline appropriate testing to diagnose the
cause of ARF
 Recommendations for treating ARF
 Case presentation
Acute Renal Failure
 An abrupt or rapid decline in renal function.
 Recognized by a rise in BUN or serum
creatinine concentrations.
 With or without a decline in urine output.
 Often transient and completely reversible.
Pathophysiology
 ARF may occur in 3 clinical settings
1. An adaptive response to severe volume
hypotension.
2. In response to cytotoxic insults to the
kidney.
3. With obstruction to the passage of urine.
Classifying ARF
 ARF is classified as oliguric or nonoliguric.
 Oliguria is defined as a daily urine volume of
less than 400 mL/d.
 Anuria is defined as a urine output of less
than 50 mL/d
 If anuria is abrupt in onset, it is suggestive of
obstruction.
Frequency of ARF
 Approximately 1% of patients admitted to
hospitals have ARF at the time of admission.
 The estimated incidence rate of ARF is 2-5%
during hospitalization.
 Approximately 95% of consultations with
nephrologists are related to ARF.
Morbidity and Mortality
 The mortality rate estimates vary from 2590%.
 The mortality rate is 40-50% in general and
70-80% in intensive care settings
History and Physical
 Hypotension
 Volume contraction
 Congestive heart failure
 Nephrotoxic drug ingestion
 History of trauma or unaccustomed exertion
 Blood loss or transfusions
History and Physical
 Evidence of connective tissue disorders
 Exposure to toxic substances such as ethyl
alcohol or ethylene glycol
 Exposure to mercury vapors, lead, or other
heavy metals, which can be encountered in
welders and miners
Causes of ARF
1. Prerenal 40-80%
2. Intrarenal 50%
3. Postrenal 5-10%
Prerenal
 Hypotension
 CHF
 Hypovolemia from renal losses
 Hypovolemia from extrarenal losses
 Vasoconstriction
Intrarenal
 Vascular causes
 Interstitial nephritis
 Glomerular factors
Postrenal
 Bladder outlet obstruction due to prostatic
hypertrophy
 Uretheral stictures
Lab studies
 BUN and creatinine
 CBC with peripheral smear
 Urinalysis
 Urine Electrolytes
BUN and Creatinine
 BUN values that increase disproportionately
larger than those of creatinine suggest
prerenal azotemia
 The ratio of BUN to creatinine greater than
20:1 suggest volume contraction.
CBC and peripheral smear
 Results can increase differential diagnosis to
include TTP, multiple myeloma, DIC
Urinalysis
 Granular muddy-brown casts—ATN
 Reddish brown colour—acute glomerular nephritis,
presence of myoglobin or HgB
 Eosinophils—UTI’s, glomerulonephritis, acute
embolic disease, drug-induced interstitial nephritis
 RBC casts—glomerular disease
 WBC—pyelonephritis, or acute interstitial nephritis
Urine Electrolytes
 Fractional excretion of sodium (FENa).
 With decreased GFR, the kidney will reabsorb salt and water
avidly if there is no intrinsic tubular dysfunction. Thus,
patients with prerenal failure should have a low fractional
excretion percent of sodium (< 1%).
 FENa = (UNa/PNa) / (UCr/PCr) X 100
 Oliguric states are more accurately assessed with this
formula than nonoliguric states because the kidneys do not
avidly reabsorb water and sodium in nonoliguric states.
Imaging studies
 Ultrasound
 Doppler scans
 Nuclear scans
 Renal biopsy
Treatment
 Balancing volume status and correcting
biochemical abnormalities.
 All nephrotoxic agents must be discontinued
or used with extreme caution.
 All medications cleared by renal excretion
should be discontinued or their doses should
be adjusted appropriately.
Treatment
 Correct acidosis with bicarbonate
administration
 Correct hyperkalemia by decreasing the
intake of potassium, delaying the absorption
of potassium, using potassium-binding
resins, controlling intracellular shifts, and
instituting dialysis if necessary
 Correct hematologic abnormalities
Case presentation
 Pt is a 47 y/o WM who presented to MCH ER via
ambulance after he was found by counselors at
stairways falling and complaining of dizziness. Pt
states unsteadiness has been going on for the past
week with associated nausea, vomiting, and change
in urine stream. Pt states he cannot hold any food
down. He denies fevers/chills or diarrhea, CP,
SOB. Pt has psych history. Pt had previously
normal renal function.
Medications











Lithium ER 450 mg bid
Promethazine 25 mg q 6hour prn
Topamax 150 po bid
Wellbutrin SR 150mg 2 in am 1 in pm
Clonidine 0.1 mg bid
Lamictal 25 mg 2 hs
Lisinopril/HCTZ 20/25 qd
Glipizide XL 5 qd
Lipitor 40 mg qd
Diltiazem 240 mg qd
Paroxetine 20mg qd
Past Medical History
 HTN
 Type II Diabetes
 Psychiatric history
 Hypercholesterolemia
LABS in ER
 BUN 81
 Creat 10.5
 Potassium 3.1
 Albumin 1.7
 Myoglobin 442
 UA yellow, hyaline casts
 Lithium 3.00 (0.60-1.20)
Admission
 Pt was admitted to ICU and was hydrated
aggressively
 Nephrology consult was obtained
 U/S was significant for R hydronephrosis
 Pt was started on dopamine drip in the ER
 CT chest with contrast was done in ER
 Urine output was good and responded nicely to
fluids
Lab studies
 Second set on day of admission
Creat 8.8
Bun 74
 Day one
BUN 63
Creat 6.4
Day four
 BUN 13
 Creat 1.1
 Patient discharged to home.
Questions or Comments