Oliguria

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Oliguria

Oct 28, 2014 0

critical care,General medicine,general surgery,intensive care,onthepods,renal

James talks to Dr Rob Hislop about the approach to oliguria, low urine output, on the wards.

Script Writer: Abhijit Pal

Summary Writer: Abhijit Pal

Editor: James Edwards

Interviewee: Rob Hislop

About Dr Rob Hislop

Dr Robert Hislop is the Intensive Care Head of Department at the Mater Hospital and Staff Specialist Intensivist at the Royal Prince Alfred Hospital, Sydney. Rob is a Clinical Lecturer at the University of Sydney and has a strong interest in Echocardiography, Clinical Governance and Quality, Healthcare in the developing world and medical education. Rob is also an active volunteer at Open Heart International.

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Oliguria

With Dr Robert Hislop (ICU Consultant at Royal Prince Alfred Hospital)

Case

You are night cover on a surgical ward, and nursing staff ask you to see a patient Day 1 post-op with poor urine output. For the last 2 hours, 20 ml/h urine output. Can you chart a fluid bolus?

Firstly, DO NOT just give 500 ml fluid stat and hope it fixes the problem. Do not just give the patient frusemide.

1. General approach

See the patient and assess them:
- Haemodynamics? Pulse? BP? JVP?
- Respiratory rate? Oxygen requirement?
Make sure IDC isn’t blocked.

2. Be aware

This is a poorly dealt with situation in hospitals! A blanket approach of giving fluids is not appropriate. Low urine output is not always due to hypovolaemia causing poor renal perfusion.
Less than 20% of patients this is the case!
Patients usually have low urine output as a physiological response to post operative stress or just being unwell in hospital.
If haemodynamics are reassuring, normotensive and well perfused – it is unlikely that this urine output represents hypovolaemia or dehydration.

3. Basic physiology

Traditionally 0.5 ml/kg/h is the cut off – Dr Hislop believes this is slightly inaccurate.
Consider the difference between obligatory and facultative urine production.
Obligatory urine – minimum urine a person has to make under maximal concentrating abilities to remove toxins (Cr, K+, H+) – in the realm of 400 ml/24 hours (but will be affected by diet).
This is how hospital patients (high ADH, high catecholamines) – 15 ml/h. (closer to 0.25 ml/kg/h). Anything below this number is very serious. True oliguria.
15 – 30 ml/h is probably OK (in the presence of normal haemodynamics).
If patient is passing less than obligatory amount of urine then they have renal dysfunction. They will develop metabolic acidosis, hyperkalemia (e.g. these are the patients who can die from hyperkalemia overnight).

4. Management

Low UO with poor haemodynamicst  then give fluid bolus (1 L N/S stat), see how the JVP changes. If the patient is volume responsive, and JVP doesn’t change and HR drops, BP rises, and urine produces – likely hypovolaemic shock.
If JVP just rises quickly (then there may be another cause of shock – tamponade, cardiogenic).
When dealing with low urine output – balancing kidneys and CV system, and CV system vs respiratory:
- If we’re giving fluid, and they are hypoxic due to pulmonary oedema –we may end up with worsening hypoxia (but if normal sats, good RR, OK probably to give fluids).

Q&A

5. Why not just give patients fluids? What’s wrong with being on the wet side?

More positive a patient’s fluid balance, worse outcome. Fluid retention and water retention have been shown to have outcomes. Fluids are a drug. Many patients get far more fluid than they need in hospital.
Maitland et al. (2011) showed that in septic children, fluid boluses in fact worsened mortality.
Fluids are helpful when appropriate, but harmful when not. Avoid the knee jerk response of IVF to low urine output.
Facultative urine production – impaired ability in patients with high ADH tone, lying supine, pain, nausea, opiates all facilitate release of ADH and we hold on to more free water (even though we thinks its inappropriate!). Patients are not good at it.
A typical (circular!) sequence of events ‐ post operative patient making 20 ml/h, nursing staff ask RMO for review of urine output, patient given volumes of fluid, next day patient is found to be hyponatremic, and on examination is euvolaemic (not hypotensive, not dehydrated, no adrenal, no heart failure, no thyroid) – diagnosed with SIADH, then fluid restrict (even though urine output hasn’t changed at all).

6. Is poor UO a canary in the mineshaft? An early marker of shock?

Another traditional area that is likely wrong.
Good urine output = good cardiac output (unlikely shocked).
But low urine output DOES NOT EQUAL shock (poor positive predictor, unless combined with associated haemodynamic compromise).
Kidneys are a complex organ and we can only simplify them so far.
Bellomo et al. (2008) demonstrated that renal blood flow can actually be increased in the setting of oliguria due to sepsis in a sheep model.
Therefore no good link between CO, GFR, and urine output (and may even be an inverse relationship).

7. Take home messages

Not all low urine output in hospitalised patients is secondary to a pre-renal cause.
Be worried if UO < 0.25 ml/kg/h or approximately < 15 ml/h (this is less than the amount they need to appropriately excrete Cr, K+, H+).
Low UO with poor haemodynamics = volume resuscitation (1L N/S and then reassess for response).
If concerned but not clear which direction to go – repeat creatinine (no renal failure) and send off a urine sodium (if pre-renal cause of low UO, urinary sodium < 10).
Frusemide is not a drug to make the UO a better number (only to treat fluid overload, hyperkalemia, acidosis).
Remember that patients are poor facultative urine producers and will not cope with excess fluid (pulmonary oedema, peripheral oedema) so think carefully, and treat fluid as a drug.

References

Bellomo, R., Wan, L., Langenberg, C. & May, C. 2008. Septic acute kidney injury: new concepts. Nephron Exp Nephrol, 109, e95‐100.
Maitland, K., Kiguli, S., Opoka, R. O., Engoru, C., Olupot‐Olupot, P., Akech, S. O., Nyeko, R., Mtove, G., Reyburn, H., Lang, T., Brent, B., Evans, J. A., Tibenderana, J. K., Crawley, J., Russell, E. C., Levin, M., Babiker, A. G. & Gibb, D. M. 2011. Mortality after fluid bolus in African children with severe infection. N Engl J Med, 364, 2483‐95.