Question 14

College Answer

Oliguria in the critically ill may well be an appropriate physiological response to relative volume depletion and circulating stress hormones (including ADH). In that scenario, there would be no evidence of renal failure per se (eg. increase in serum creatinine, decreased creatinine clearance), appropriate urinary concentration would occur (elevated urinary specific gravity and osmolality andlow urinary sodium <20 mmol/L), and an increase in urine output would be expected with fluid loading and/or diuretic administration. If instead signs/investigations suggest renal failure is developing, this would be traditionally divided into pre-renal, renal and post-renal causes. History (e.g. deliberate fluid restriction, associated medical conditions, past history of abdominal surgery, muscle damage, administration of nephrotoxic drugs [e.g. NSAIDs] etc.) and examination (confirmation of diagnosis [e.g. palpation, catheterisation, bladder scan], dehydrated, abdominal distension with increased intra-abdominal pressure, blocked/misplaced urinary catheter, etc.) will obviously help in the diagnosis. Urinalysis is also helpful (e.g. granular or epithelial cell casts with acute tubular necrosis, active sediment with glomerulonephritis, heavy proteinuria with nephritic syndrome.  Further  monitoring  may  be  required  if  the  haemodynamic  status  is  considered inadequate, and specific investigations to assess renal blood flow or exclude obstruction may be clinically indicated.

Specific treatment will depend on the cause (e.g. optimise pre-renal state with hydration and/or haemodynamic  supports,  adequate  treatment  of  infection,  relieve  obstruction,  remove nephrotoxins), but in general there are no specific therapies that have been demonstrated to improve long-term outcome. Treatment options that could be considered include diuretics to enhance urine output, alkalinisation of urine for rhabdomyolysis, and CRRT rather than intermittent haemodialysis if indications for dialysis have been met.

Discussion

An excellent article on evaluation of oliguria in the ICU is presented by RN Sladen.

A systematic aproach to oliguria is summarised elsewhere.

Briefly, an approach to this specific scenario would resemble the following:

1) Confirm oliguria.

• Exclude IDC malposition or kinking

2) Discriminate between renal success and renal failure.

• Oliguria may be the manifestation of normal volume conservation mechanisms:
  • History will suggest decreased fluid intake
    • Vasopressin use may also be an obvious clue
  • Examination will demonstrate features of dehydration
  • Biochemistry will show an increased urea/creatinine ratio
  • Urinalysis will reveal concentrated urine with low urinary sodium
• Such oliguria will also respond to fluid boluses.
• Oliguria in the presence of normal or increased fluid balance suggests a failure of normal renal excretory function.
• Hypovolemia and dehydration may also be associated with renal failure; a failure to respond to fluid boluses can be an indication that pre-renal failure has developed. Oliguria of normal renal fluid conservation in hpovolemia is a continuum with the oliguria of renal failure due to renal hypoperfusion, and these categories may overlap.

3) Discriminate between causes of renal failure

• Pre-renal causes
  • History and examination may suggest CCF, cirrhosis, renal artery stenosis, and so on.
  • Haemodynamic parameters may suggest decreased cardiac output and decreased renal perfusion
  • Hypovolemia due to dehydration may be supported by the serum biochemistry
  • Imaging of the renal vasculature may reveal stenosis or renal vein thrombosis
  • Urinalysis in this case should reveal no specific findings
  • Non-specific management would consist of optimising hemodynamic performance to improve renal perfusion.
  • Specific management would be dependent on the specific aetiology.
• Intrarenal causes
  • History would reveal trauma, infection, or the use of nephrotoxic agents.
  • Examination may confirm a source of sepsis
  • Biochemistry may demonstrate hypoprotinaemia (in nephrotic syndrome), a raised CK (rhabdomyolysis) or metabolic acidosis.
  • Specific biochemistry (ASOT) may reveal post-streptococcal glomerulonephritis as the cause of renal failure. Similarly, anti-GBM antibodies may confirm Goodpasture's syndrome.
  • Urinalysis is useful:
    • Muddy brown casts may suggest ATN
    • Proteinuria may suggest nephrotic syndrome
    • Red cell fragments may suggest glomerulonephritis
  • Non-specific management would consist of optimising hemodynamic performance to improve renal perfusion.
  • Specific management would be dependent on the specific aetiology, be it forced diuresis for rhabdomyolysis or high-dose steroids for Goodpasture's.
• Post-renal causes
  • One must consider an obstruction of the urinary tract:
    • Ureteric obstruction by calculi or infection
    • Ureteric stenosis due to prior radiotherapy
    • Ureteric or bladder injury
    • Urethral obstruction by kinked or malpositioned IDC.
  • Management would be specifically targeted to relieve the obstruction, and would depend on the nature and location of the obstruction. The range includes percutaneous nephrostomy, ureteric stenting, ureteric diversion, or simply reinserting the IDC.

Sladen, Robert N. "Oliguria in the ICU: systematic approach to diagnosis and treatment." Anesthesiology Clinics of North America 18.4 (2000): 739-752. This article is perfect for this question, but is not available as free full-text.

Lesko, Janene, and James R. Johnston. "Oliguria." AACN Advanced Critical Care 8.3 (1997): 459-468.

Dujovny, Nadav. "Oliguria." Common Surgical Diseases. Springer New York, 2008. 367-369.

Zaloga, Gary P., and Steven S. Hughes. "Oliguria in patients with normal renal function." Anesthesiology 72.4 (1990): 598-602.