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SAMIR EL ANSARY

Oliguria -f

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Page 1: Oliguria  -f

SAMIR EL ANSARY

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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

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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

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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

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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

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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)◦ Foley catheter obstruction

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-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

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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

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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

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-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)

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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

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-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).

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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

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Prerenal:◦ Treat underlying cause◦ If volume depleted (see physical exam): NS

boluses (500-1000ml f luid 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).

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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)

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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.

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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.

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GOOD LUCK

SAMIR EL ANSARY