1. DECREASED URINE OUTPUT (Oliguria and Anuria)
Matthew Glassy
Mini-Lecture Powerpoints
4/2014
- This discussion will focus on acute causes of decreased urine output

2. OBJECTIVES Learn the definition of oliguria/anuria
Learn an approach to decreased urine output
Learn to assess a pts Foley status when first approaching decreased urine output

3. Case
56 yo M h/o COPD, HTN, HLD, OSA who is admitted for cellulitis, started on vancomycin and zosyn and fluid resuscitated to euvolemia. His WBC was 18k, lactate 2.3 and Cr 1.4 on admission. Cr 0.9 on HD 2. On HD 4 you are paged by the RN who tells you that the pt has had decreased UOP since her shift.

4. DEFENITION Oliguria = Urine output <400cc/day (<17cc/hr)
OR urine output <0.5ml/kg/hr
Anuria = Urine output <50-100cc/day
Always first consider urinary tract obstruction (i.e., foley or bladder outlet obstruction)
When first paged about decreased urine output, important to ask about/calculate exact urine output, as decreased urine output does not signify oliguria and urine output may still be in normal range.

5. QUICK CONSIDERATIONS YES NO FLUSH FOLEY CATHETER WITH 30-50cc NS
OBTAIN PVR
OR I/O CATH
URINE OUTPUT IMPROVED?
PVR ≥ ?
FOLEY LIKELY CLOGGED WITH SEDIMENT
PROCEDE WITH FURTHER WORKUP
START FOLEY & PROCEDE W/ FURTHER MANAGEMENT
PROCEED WITH FURTHER WORKUP
Does the patient have a foley catheter?
- Urinary tract obstruction occurs in <5% of cases of ARF, but it is often reversible and should be ruled out early in the evaluation
If pt does not have foley catheter, you may consider the accuracy of decreased urine output assessment (ie. Any undocumented bathroom visits by the pt, are the bed sheets wet?, is any urine spilled onto bed/floor or flushed before quantifying?)
Note: Always review the already available imaging such as CT scans jumping to ordering renal US’s

6. ETIOLOGIES TO CONSIDER
Prerenal:
Decreased circulatory volume – dehydration, hemorrhage, burns
Reduced cardiac output – CHF, tamponade, constrictive pericarditis
Sepsis/shock/vasodilatation
Volume sequestration – pancreatitis, peritonitis
Drugs – diuretics, NSAIDS, ACE/ARB
Renal vasoconstriction – severe heart failure, hepatorenal, NSAIDS
Intrarenal:
ATN – ischemic and toxic
AIN – drugs, infections, autoimmune diseases
Glomerulonephritis
Microvasculature Injury – HUS/TTP, DIC, malignant HTN
Renal artery /vein occlusion – thromboemboli, atheroemboli, aortic dissection
Postrenal:
B/l ureteric obstruction (stones, clots, tumors, fibrosis)
Bladder outlet obstruction (BPH, tumors/retroperitoneal mass, clots)
Foley catheter obstruction
Decreased renal perfusion or pre-renal accounts for 40-80% of causes of ARF, and if appropriately treated, is readily reversible
Keep cardiorenal and heptorenal etiologies in mind with your CHF and cirrhosis patients.
When prerenal and postrenal etiologies have been excluded, an intrinsic parenchymal renal disease is present

7. CHART REVIEW
Always review chart to look for clues that may elicit etiology (see previous slide)
History: sepsis, CHF, cirrhosis, tumors, CKD, foley, recent IV contrast or hypotension episodes, allergies, etc
Meds: diuretics, ACE, vancomycin, antibiotics, iv contrast, NSAIDs
Labs: BUN/Cr (ratio), UA, urine lytes, blood cultures; vanco trough levels
Imaging: Any recent CT scans, Xrays, US
After confirming oliguria/anuria, evaluating if pt has a foley, and considering etiologic categories, the next step is a chart review:
Don’t forget to review any imaging already available such as new and old CT’s/US’s

8. EXAMINE THE PATIENT Obtain new vitals, including orthostatics
Look for:
Volume status
Dry MM, decreased capillary refill, skin tenting
JVP or CVP if central line
Crackles, pleural effusions, LE edema
Ascites
Ideally bedside US of IVC for evidence of low/high cardiac filling P
Evidence of Cirrhosis
Examine foley and urine sediment in foley
Make sure pt has not wet the bed with unaccounted for UOP
Palpate Kidneys and Bladder
Rashes and other skin lesions
-Vitals: +orthostatics can clue into hypovolemia even if BP is normal while lying
-Signs of cirrhosis – hepatorenal syndrome?
-Ideally a bedside US of IVC with provide high or low cardiac filling pressures that will help asses fluid status and CHF
-Rash (AIN, embolic renal failure, HUS/TTP, DIC, etc)

9. Case
56 yo M h/o COPD, HTN, HLD, OSA who is admitted for cellulitis, started on vancomycin and zosyn and fluid resuscitated to euvolemia. His WBC was 18k, lactate 2.3 and Cr 1.4 on admission. Cr 0.9 on HD 2. On HD 4 you are paged by the RN who tells you that the pt has had decreased UOP since her shift.

10. Back to Our Case Does he have a foley?
No, and his PVR is 30 cc
Does he really have decreased urine output?
His calculated UOP has been 300cc over last 24 hour, previous was 1600cc/day. No unaccounted for UOP after questioning RN and examining if the bed is wet
Chart review:
Currently not on any fluids; cellulitis markedly improved; WBC 8k this am
Cr is 2.2 this am
No periods of hypotension, received 5L NS total since admission
Recent echo with EF 55%, CXR without vascular congestion on admission
Vanco trough was yesterday (first trough was 10.5)
CT abd/pelvis with contrast, done in ER, shows no hydro and normal size b/l kidneys
Received IV contrast on admission 4 days ago
UA on admission w/o any abnormalities
See next slide for notes on this and the next slide.

11. Back to Our Case Physical exam:
BP 139/76, HR 78, RR 17, sating 96% RA, Temp 99.6,
NAD, non-toxic.
MMM, cap refill < 2 sec, no skin tenting
No JVD, lungs clear, no edema. IVC not dilated on bedside US and >50% resp variation.
No ascites or jaundice.
No bladder distension or CVA TTP.
+fine confluent macular rash over chest.
These are note for this and the previous slide:
Are we concerned for urinary obstruction? No PVR is only 30cc and our exam did not detect bladder distension
What etiologies are we still considering?
Pre-renal - Sepsis (Does not appear so) vs dehydration (euvolemic on exam) vs CHF (no).
Intrinsic renal; DDx: vancomycin (trough is on lower end) vs contrast (possibly but usually will manifest on day 2) vs other intrinsic renal.
We will need further studies to know more precisely that this is an intrinsic renal etiology

12. MANAGEMENT If not already done order (to help classify etiology):
Basic electrolytes, CMP (monitor changes in Cr/GFR, LFTs, albumin), urine studies (U/A, Na, Cr, urea, eos), UCx
Consider further kidney imaging
Adjust/replace/discontinue nephrotoxic agents. Renally dose the non-toxic meds
-After completing all previous work so far were are left with a likely intrinsic renal etiology which needs further management to diagnose and treat
-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. Back to Our Case Urine sample shows: Further management:
UA: WBC hpf, neg LE/nitrite, 3-4 RBC hpf, 1+ protein
Urine studies: UNa 80, UCr 30, FENa = 4.3%
UCx: no growth after 2 days
Urine Eos: Positive
Some WBC casts, no other casts
Further management:
Do you want to order any imaging?
Do you want to change any medications?
-What is our pts urine sample consistent with, a pre-renal or intrinsic renal etiology? Intrinsic Renal with FENa 4.3%. Also +urine Eosinophils help us determine cause
-Do you want to order imaging? We do not want to order further imaging since we already have an admission CT scan showing normal kidneys. Both acute renal failure and acute hydro will not yet manifest on imaging.
-Do you want to change any meds? Appears as though there is an AIN etiology here. We should stop both vancomycin and zosyn as both these agents are known to cause AIN. Also we should search for other potential medications that may be causing. Note, we do not have to have to the full triad of fever, eosinophillia and rash for AIN.
-Note, oliguria can occur in up to 50% of pts with AIN. Mainstay of rx is removal of the offending agent.

14. MANAGEMENT cont… Prerenal: Postrenal: Intrarenal:
Treat underlying cause
Avoid/be very cautious about giving lasix (investigation of underlying cause should drive this decision).
If volume depleted: NS boluses ( ml fluid challenges) – can repeat until response (but need to monitor for fluid overload)
Postrenal:
Initiate Foley catheter (clear/flush catheter if already in place)
1st review already available imaging ,then consider renal US to assess upper urinary tract if no other imaging already available
Intrarenal:
Remove nephrotoxins
Consider fluids for select cases – rhabdo, cisplatin toxicity, etc
-Prerenal: Always give fluids unless there is CHF or pulmonary edema (you may have to look at several previous CXRs to determine)
-Postrenal: usually expect ~500cc output after foley catheterization, and may develop post obstructive diuresis which may require large volume of IVFs
-Intrarenal: Goal is to prevent underlying cause and maintain renal perfusion (optimize MAP and CO).

15. SUMMARY Oliguria does not simply mean give a fluid bolus or lasix
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.
Avoid ordering imaging of the kidneys if there is CT or US already available – additional imaging will not help find hydro
Ultimately, regardless of pathophysiology, treating underlying cause is key for both acute and long term management.