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SAMIR EL ANSARY
 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
 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
 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
 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
 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)
-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
 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
 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
-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)
 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
-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).
 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
 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).
 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)
 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.
 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.
GOOD
LUCK
SAMIR EL ANSARY

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Oliguria -f

  • 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.