- Oliguria is defined as urine output <400cc/day and can be caused by pre-renal, intrinsic renal, or post-renal factors. - An initial assessment of oliguria includes verifying urine output, flushing any Foley catheter, obtaining a bladder scan if no catheter, and reviewing the patient's chart and conducting a physical exam to identify potential causes. - Life-threatening complications of oliguria like hyperkalemia and acidosis must be promptly recognized and managed while the underlying cause is treated. Fluid boluses can be tried for pre-renal causes but lasix should generally be avoided until the etiology is clear.

1. SAMIR EL ANSARY

2.  Definition of decreased urine output
(oliguria)
 Questions to consider when first
presented with oliguria
 Recognizing causes of oliguria
 Focused review of history and physical
 Management of oliguria
◦ Recognizing life threatening
complications

3.  Oliguria = Urine output <400cc/day
(<20cc/hr)
◦ Another def: urine output <0.5ml/kg/hr
 Anuria = no urine output
◦ Can signify complete mechanical
obstruction of bladder outlet or a blocked
Foley

4.  Does the pt have a foley catheter?
YES NO
FLUSH FOLEY CATHETER
WITH 30-50CC NS
OBTAIN PVR (w/ US or cath
[will provide urine sample])
URINE OUTPUT IMPROVED? PVR ≥ 100? (≥ 50 in younger pts)
YESYES NO NO
FOLEY LIKELY
CLOGGED
WITH
SEDIMENT
PROCEDE
WITH
FURTHER
MANAGEMENT
START FOLEY
& PROCEDE W/
FURTHER
MANAGEMENT
PROCEED
WITH
FURTHER
MANAGEMENT

5.  Consider the pathophysiology/causes of
decreased urine output. Three categories of
causes:
 Prerenal:
◦ Volume depletion/dehydration/inadequate fluid
maintenance/Infection/sepsis
◦ Reduced cardiac output
 ICU setting: mechanical ventilation can
also lead to low cardiac output
◦ Drugs
◦ Does the pt have liver cirrhosis

6.  Intrarenal:
◦ ATN
 ICU settings: Circulator shock, severe
sepsis, multiorgan failure
◦ AIN
◦ Renal artery thrombosis/Emboli (septic
[endocarditis]
 Postrenal:
◦ B/l ureteric obstruction (stones, clots, tumors,
fibrosis)
◦ Bladder outlet obstruction (BPH,
tumors/retroperitoneal mass, clots)

7. -Reduced cardiac output examples: CHF;
cardiac temponade; constrictive pericarditis.
-Drugs that may decrease renal perfusion:
Diuretics, ACE, NSAIDS, immunosuppressive
(cyclosporine)
-Why consider liver function? Hepatorenal
syndrome
-ATN: hypotension; nephrotoxins (contrast,
myoglobin, uric acid, amyloid …etc)
-AIN: drugs (antibiotics, NSAIDS, diuretics),
infection

8.  Review chart to look for clues that may elicit
etiology (see previous slide)
 History (sepsis, CHF, tumors, renal failure…etc)
 Meds: diuretics, ace,
aminoglycosides/vancomycin, iv contrast, NSAIDs
 Old Labs: BUN/Cr (ratio); urine lytes; blood
cultures; vanco trough levels

9.  Obtain new vitals, including orthostatics
 Look for:
◦ Jaundice
◦ Crackles, pleural effusion
◦ JVP, CVP if pt has central line
 Especially useful in ICU for pt with central line: for
example a CVP of 2 can be good evidence for
hypovolemia
◦ Palpate Kidneys and Bladder
◦ Prostate/Cervical Exam
◦ Rash

10. -Vitals: orthostatics can signify hypovolemia;
Tachycardia - hypovolemia/infection; Fever –
infection/UTI
-Jaundice (liver cirrhosis – hepatorenal)
-Crackles, pleural effusion (CHF, volume
overload)
-JVP, CVP if pt has central line (will help assess
fluid status)
-Palpate Kidneys and Bladder (hydronephrosis,
enlargement in obstruction/post-renal)
-Prostate/Cervical Exam (again for
obstruction/post-renal)
-Rash (AIN, embolic renal failure)

11.  If not already done, order basic
electrolytes, CMP (monitor changes in
Cr/GFR), and urine studies (U/A, Na,
BUN, Cr), to further help classify etiology
 Adjust/replace/discontinue and
nephrotoxic agents. Also, renally dose the
non-toxic meds

12. -Urine studies: U/A – look for proteinuria,
hematuria, eosinophilia, evidence of
rhabdomyolysis,
RBC/WBC/Granular/Pigmented/epithelial
casts…etc.
-Urine lytes: e.g. urine sodium <20
(prerenal), FENa: <1? Vs >2%/ FeUrea: <35?
-Note: On CMP look for presence and degree
of renal insufficiency.
Also look for possible complications (especially one that can
be life threatening) of renal insufficiency (e.g. hyperkalemia,
metabolic acidosis…etc).

13.  Early recognition and intervention of potential
life threatening complications (direct or indirect
causes – e.g. renal failure) is essential
◦ Hyperkalemia: obtain EKG if elevated
◦ CHF/Pulmonary Edema
◦ Metabolic acidosis; Uremia (encephalopathy,
pericarditis)
◦ Advanced complications of above may require dialysis

14.  Prerenal:
◦ Treat underlying cause
◦ If volume depleted (see physical exam): NS
boluses (500-1000ml fluid challenges) –
can repeat until response (but need to
monitor for fluid overload)
◦ Avoid/be very cautious about giving
lasix (again investigation of underlying
cause should drive this decision).

15.  Postrenal:
◦ Treat underlying cause
◦ Initiate Foley catheter (clear/flush
catheter if already in place)
◦ Obtain Renal Ultrasound to assess for
upper urinary tract problems
 Intrarenal:
◦ Treat underlying causes (e.g. sever
sepsis/shock)

16.  Verify urine output w/ definition of oliguria in
mind.
 If pt has a Foley catheter, flushing Foley is a
good initial step. If no Foley, a PVR can help
assess the need for Foley.
 A focused chart review along with a focused
history and physical can help clue in on the
pathophysiology including pre-
renal/intrinsic/post-renal causes.
 Recognizing life threatening complications (e.g.
hyperkalemia, acidosis, uremia) is an essential
component of acute/early management.

17.  Decreased urine output does NOT mean
lasix deficiency. Administering lasix may
actually exacerbate problem. However very
specific causes may require lasix.
 Fluid boluse(s) is a good initial step (be very
cautious in CHF).
 Ultimately, regardless of pathophysiology,
treating underlying cause is key for both
acute and long term management.

18. GOOD
LUCK
SAMIR EL ANSARY