Oliguria

DEFINITION
Low urine output accompanied by rapid and potentially reversible decline in kidney function.

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INCIDENCE
Incidence
A common post op problem.
- may complicate as many as 5% of admissions.
(commonly multifactorial).

Exacerbating risk factors
NSAIDs
Contrast
Aminoglycosides
ACE inhibition
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AETIOLOGY

Pathogenesis

Pre-renal, renal, post-renal.

Pre-renal
Low renal perfusion:
- see the causes of shock
- also vascular causes, eg bilateral arteritis, atheroma or stenosis

Renal:
As for renal disease.

Post-renal:
Obstruction.
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BIOLOGICAL BEHAVIOUR

Physiology
Urine output
The minimal adult urine production per day is approximately 500ml/day
- this allows the obligatory solute / acid-base homeostasis
- solute load is around 600mosmol, and max concentrating ability at 1200mosmol/kg water.
- in trauma, surgery, sepsis there may be an increased solute load requiring greater volumes of urine to be excreted.

Definitions


Normal urine output: 1ml/kg/hr
Oliguria: <400 ml/day (adult)
Anuria: <100 ml/day (adult)

Natural History

Renal response to hypoperfusion

Early
Intense Na+ conservation
--> urinary sodium <20mmol/L (unless recent diuretic)
--> water conservation
--> urine osmolarity >500 mOsm/kgH20
--> UrineCr:PlasmaCr>40 (excretory function preserved).

Tubular dysfunction

Loss of medullary concentrating power
--> urine Na+ rises
--> eventually isothenuric urine produced

Acute tubular necrosis
Tubular cell damage
--> oliguria / anuria

Pathophysiology

The tubular cells of medulla are very sensitive to ischaemia or hypoxia because they already operate at the very limit of oxidative cellular metabolism.
- the thick ascending loop cells are most vulnerable
- the underperfused kidney is much more sensitive to other insults also.

Renal hypoperfusion


Early
Renal blood flow falls
--> autoregulation:
- vasodilation of afferent arteriole and proximal renal circulation
- increased (angiotensin II mediated) efferent tone
--> renal perfusion maintained
--> GFR maintained
Aldosterone and ADH produced in response to these dynamics
--> salt &H20 retention
--> concentrated urine

Tubular dysfunction
Autoregulation progressively fails
Sympathetic innervation, angiotensin II, endothelin, PGs, ADH, and loss of endogenous vasodilators:
--> renal microvascular constriction
--> renal shut down
--> prox tubule fails to resorb Na+ and H20
- hence more fluid delivered to macula densa
--> afferent arteriolar vasoconstriction
--> helps systemic BP
--> but decreases renal blood flow further
--> ischaemia of tubule epithelium
--> unable to conserve Na+/H20.
--> Urine becomes isothenuric (urine Na+ >40mmol/L)

Acute Tubular Necrosis
The medulla is particularly sensitive to ischaemia
- pO2 in the medulla is low even in physiological conditions (20mmHg) due to metabolic activity, limited blood supply, and drawing out of O2 by countercurrent.
Injury then necrosis of the epithelium correlates with degree of insult
Viscious cycle ensues:
- GFR drops due to vasoconstriction
--> tubules become obstructed by casts, back leakage of filtrate through highly permeable tubules
--> GFR drops further

Pathology
ATN is a histological diagnosis, seen as non-specific renal injury.

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MANIFESTATIONS

Clinical Correlates

Early
Oliguria
[Na+]<20mmol/L
Osmolarity>500mOsm/kgH20
Plasma urea elevated disproportionately

Tubular Dysfunction
Loss of urinary concentration
[Na+]<20mmol (prox tubule fx preserved)
- but GFR reduced:
Osmolarity <350
Renal recovery will take several days

Acute Tubular Necrosis
Isothenuria
[Na+]>40mmol/L
Osmolarity <350
- similar to plasma
GFR reduced to <5ml/min
Long time before renal recovery
- may need dialysis.

Clinical Assessment
(for hypovolaemia)

?Blocked catheter


?Falling BP, rising pulse
- over hours / days
- periods of hypotension intra/post op
- remember many older pts may be hypertensive

?Negative balance
- inadequate fluid replacement
- large GI losses
- excessive wound drainage
- frequent dressing changes due to haemorrhage
- decreasing daily weight
- inappropriate diuretic administration

?Nephrotoxic drugs

- see incidence above

?Clinical features of low perfusion
- thirst, dry mouth, cold peripheries, guttered veins
- orthostatic hypotension (normotension is not sensitive)
- JVP (lie pt head-down if needed)

?Third spacing
- eg ascites, pleural effusion, oedema, soft tissue injury



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INVESTIGATIONS
Imaging
CXR may confirm hypervolaemia but useless for hypovolaemia

Fluid Challenge
The way to confirm hypovolaemia
Infust 250ml 0.9% saline or colloid over 10mins.
Monitor BP/JVP/CVP/PAWP as possible
If hypovolaemic:
--> correction of reduced values within 20-30mins but transient.
If euvolaemic:
--> sustained rise in pressures.

Diagnosis
Four tests diagnose cause of oliguria:
(besides clinical means)
1. Creatinine
- see ARF notes for detail
2. Urinary sodium
- ?renal hypoperfusion
3. Urinalysis & microscopy
- ?primary renal cause
 - mandatory if suspected.
- eg may show granular casts, dysmorphic RBCs of glomerulonephritis.
- deeply pigmented casts in pigmenturias like rhabdomyolysis.
- eosinophilia / urine WC casts may suggest interstitial nephritis.
4. Renal imaging
- ? renal abnormality
- ?renovascular insufficiency due to vessel occlusion.

Other
Read the notes - what is the pt's cardiovascular status?
- have they had contrast recently?
- is there a chance of rhabdomyolysis?
- recent blood transfusion?
Read an ECG.
Do a Trop if indicated.
Examine/check for sepsis.
- investigate sources as indicated.

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MANAGEMENT

See also ARF
- if anuric / obstructed see ARF notes.

Prevention
Is most important.
Identify at risk pts.
Avoid nephrotoxins.
Infuse them pre-op.
And adequately perfuse them post op

The 5 Rules of Renal Failure (CCrISP)
1. Kidneys need adequate perfusion
2. Perfusion depends on adequate BP
3. A surgical pt with low urine output usually requires more fluid.
4. Absolute anuria is most often due to urinary tract obstruction.
5. Poor urine output is not due to frusemide deficiency.
- and there is no evidence achieving diuresis in early stages of renal failure will help renal recovery.

1. Correct Hypovolaemia
As rapidly as possible.
- use salt-containing fluid eg colloid or normal saline.
- do not replace excessively so as to overload.
- there is no evidence that low dose frusemide or mannitol or dopamine has any role.
- add O2 to keep cells tubular cells well oxygenated

2.  If oliguria persists:
Measure urinary sodium.

Then eg: (think).
<20 mmol/L (pre-renal/medullary hypoperfusion)
- ? pre-renal cardiovascular cause
- ? renal cause eg drugs, rhabdomyolysis

>40 mmol/L
  (ATN)
- ?renal parenchymal disease
- ?renal severe nephrotoxicity
- ?obstruction ie post renal seive.

And undertake investigations for cause

3. Stop nephrotoxic drugs
- eg Gent, NSAIDs, ACEi, opioids, B-blockers.
- also contrast media
- also modify the dosing interval of any drug renally excreted.

4. Optimise cardiac output
Fluids, inotropes, vasodilators, anti-arryhthmics may be reqd.

5. Treat contributing causes
Eg correction of underlying surgical condition such as ischaemic gut, sepsis or ischaemic leg.

6. The non-progressing pt
If there is no rapid response:
- transfer to HDU setting
- insert a CVP line to ensure circulation is full
- consider an inotrope (with invasive BP monitoring) to maintain MAP to perfuse kidneys.
If the pt is still passing into established renal failure:
- urine sodium concentration may be elevating to suggest this.
--> see ARF, renal replacement therapy may be required.

Prognosis
About 95% of ATN pts will recover renal fx in 6 wks.
- some will subsequently develop chronic renal failure.
- even after 12 months apparently normal pts are at risk of ATN again as defective concentration and acidification in kidney.
As many as 50% of acute renal failure pts with ATN will die.

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