DECREASED URINE OUTPUT ( Oliguria and Anuria )

1. DECREASED URINE OUTPUT (Oliguria and Anuria) Matthew Glassy Mini-Lecture Powerpoints 4/2014

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)

5. QUICK CONSIDERATIONS Does the patient have a foley catheter? NO YES FLUSH FOLEY CATHETER WITH 30-50cc NS OBTAIN PVR OR I/O CATH PVR ≥ 200-300? URINE OUTPUT IMPROVED? YES NO YES NO FOLEY LIKELY CLOGGED WITH SEDIMENT PROCEDE WITH FURTHER WORKUP START FOLEY & PROCEDE W/ FURTHER MANAGEMENT PROCEED WITH FURTHER WORKUP

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

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

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

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 15.5 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

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.

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

13. Back to Our Case • Urine sample shows: • UA: 5-10 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?

14. MANAGEMENT cont… • Prerenal: • Treat underlying cause • Avoid/be very cautious about giving lasix (investigation of underlying cause should drive this decision). • If volume depleted: NS boluses (500-1000ml fluid challenges) – can repeat until response (but need to monitor for fluid overload) • Postrenal: • Treat underlying cause • 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: • Treat underlying cause • Remove nephrotoxins • Consider fluids for select cases – rhabdo, cisplatin toxicity, etc

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.