Oliguria

 It is the low output of urine

 80-400mL/day
 1mL/kg/h in an infant
 <0.5mL/kg/hr in a child
 <400-500mLday for adult aka 17-21mL/hr aka 0.2-0.3 OR 0.5mL/kg/hr
 Anuria is usually defined aty <100ml/day
 It is usually not a concern unless ARF is also present
 This is a significant (>50%) decrease in GFR with an associated accumulation of nitrogenous
wastes (UEC/BUN/creatinine) in the body aka axotemia
 Serum creatinine is the most accurate estimate of GFR
 ARD = serum creatinine increase more than 0.5mg/dL; normal 0.8-1.4
 Post operatively
 It si a common problem and is usually due to the failure of the medical team to appreciate
the volume of fluid lost by the patient during the surgical procedure and in the immediate
post-operative period
 It is important to ensure that the patient is not under urinary retention before classifying it
as due to decrease urine output
 If there is any doubt, insert a catheter or USS bladder to determine bladder content

Causes
 Dehydration
 Renal failure
 Hypovolaemic shock
 HHNS
 Multiple organ dysfunction syndrome
 Obstruction or urinary retention
 DKA
 Pre-clampsia
 UTI

Pre-renal
 This is the most common cause of oliguria
 Hypoperfusion of the kidney - hypovolaemia, pump failure or pre-renal failure
 Decrease is blood volume
 Dehydration
 Poor intake
 Haemorrhage
 GI losses
 diarrhoea
 Decrease PO
 Relative decrease in blood volume
 Cardiogenic shock
 Vasodilators
 Renal artery stenosis
 G6PD deficiency
  Sepsis
Renal
 Due to renal damage
 Hypoperfusion
 Rhabdomyolysis
 Medications
 Acute glomerulonephritis
 Interstitial nephritis
 Acute tubular necrosis
 Ischaemia
 Drugs
 toxins
Post-renal
 post renal failure
 As a consequence….
 Obstruction
 Calculi
 Tumour
 Obstructed foley catheter

Dx
 Perform USS renal to rule out obstructive processes

In the post-op patient

 Patients will often have diminished urine output after a major operation
 This can be due to fluid and blood loss and the response of the adrenal cortex to stress
 There is increase aldosterone release and ADH released in the first 24hrs post operation
 This results in both salt and water retention
 The oliguria should be temporary and not last more than 24hrs
 If there is urine output of less than 400mL in the first 24hrs then this needs Ix
 Major surgery with large intra-operative fluid loss and periods of hypotension during the
procedure might suggest renal tissue damage  renal tubular necrosis
 Severe peritonitis with large fluid shift and no hypotension  inadequate fluid replacement

How to assess a patient with oliguria

 Review the patient
 Resuscitation needed?
 ABCs
 Hx
 Suspect acute renal damage if the patient has been exposed to a prolonged time of oliguria
or has nephrotoxic drugs
 Does the patient have any sx or predisposing conditions that suggest hypovolaemia
 Diarrhoea
 Vomiting
 GI bleeding
 Fever
  Low intake – IV or oral
 Positional dizziness
 Dizziness suggests hypovoalemia
 If post op- bleeding, wound drainage, infection leading to septicaemia
 Are there any previous sx suggestive of bladder outlet obstruction from prostatic
hypertrophy
 Hesitancy
 Difficulty voiding
 Dribbling
 I.e. rule out post renal obstruction
 Any Hx of haematuria
 Renal stones leading to obstruction
 Sx of acute renal failure
 Previous Hx
 Renal disease
 Nephrotoxic drugs or agents
 Aminoglucoside AB
 NSAIDs
 Contrast for imaging
 Chemotherapy
 Any underlying disease or procedures that could result in oliguria
 Cardiac failure
 Cirrhosis
 Epidural infusion
 Sx suggestive of uraemia
 Nausea
 Vomiting
 Anorexia
 Insomnia
 Mental status changes
 Exam
 Vital signs
 ABC
 Decrease weight suggests volume depletion
 Hypertension
 Volume overload
 If chronic then cause for renal insufficiency
 Orthostatic BP  check for it
 Pulse
 AF is a common cause of emboli
 HR
 BP supine and erect
 SatO2%
 RR
 General
 Does the patient look well or unwell
  Are they alert and orientated
 Skin
 Decrease skin tugor or dry mucous membranes suggest hypovolaemia
 Head and Neck
 Flat neck veins while supine  voume depletion
 Raised JVP in volume overload
 Tongue – dry vs moist
 Chest
 Rales -> CHF
 Pitting sacral oedema
 Abdomen
 Ascites
 Cirrhosis
 CHF
 Distended bladder (palpate)
 Outlet obstruction
 G/U
 PR for male’s prostate
 Pelvic exam for females
 Extremities
 Assess perfusion
 Colour
 Capillary refill
 Temp
 Pitting oedema (lower limb)
 Other
 Inspect the operative site
 Inspect drains
 Flush catheters
 Ix
 FBC
 Haemorrhage
 CXR
 Heart failure
 ECG
 Heart failure
 Arrhythmia
 Ischaemic changes
 Septic screen
 Febrile patients
 Urea, creatinine and electrolytes
 Urinalysis
 High specific gravity
 Volume depletion
 Large amounts fo protein or red cell casts
 Glomerular disease
  Haematuria – significant
 Renal emboli or stones
 WBC casts
 Infection
 Severe inflammation
 Granular casts
 Acute tubular necrosis
 Serum chemistries
 Compare blood urea with creatinine
 If ratio >10:1; prenal cause is likely but it could also be an obstruction. GI bleeding,
severe catabolic state
 If ratio <10:1; renal cause is likely
 Always note high/low sodium or high potassium which can complicate acute renal
failure
 Urine electrolytes and creatinine
 Urinary sodium <15mmol/L suggests pre-renal
 >20 suggests renal

Signs of shock
 Early
 Tachycardia  beware of b Blockers
 Postural drop in BP
 Increase RR
 Late
 SBP <HR
 Oliguria
 Very late
 Bradycardia
 Confusion
 Glasgow coma scale score decrease

Mx
 Only proceed if confident about the diagnosis, otherwise call for help
 NOTe that aliguria in an alert patient that is associated with normal pre-existing renal functions
and CVS is unlikely to require intervention unless it persists for 4+ hours
 If oliguria is associated with other sx suggestive of fluid depletion, tx with fluid challenge
 It is important to exclude obstruction of the UT or catheter in all cases
 Diretics should not be used to treat oliguria and should be reserved for fluid overload
 Dopamine should not be used to treat oliguria or to prevent renal failure
 Minimal acceptable output is 1mL/kg/hr
 Take records of fluid intake and output
 Review medications and stop all nephrotoxic drugs
 Aminoglycosides
 NSAIDs
 COX-2 inhibitors
 Adjust the doses of all renally excretd drugs
 Address all the septic foci
 Abx
 Surgical drain
 UTI
 If pre-renal
 Volume challenge
 500mL NS for 30min
 Monitor volume replacement to ensure circulatory adequacy (ie. Use arterial and R heart
catheters to emasure CVP to be above 10mmHg)
 Follow hourly urine output with a urinary catheter
 Consider additional measures
 Frusemide – usually if there is a fluid overload
 Pre-renal hypovolaemia fluid replacement
 Poor output due to pump failure  diuretic therapy and possible medications (inotropes,
antiarrhythmics) to improve cardiac function
 DO NOT GIVE HYPOVOLAEMIC PATIENT A DIURETIC. Diuretics are used to treat fluid
overload

In acute renal failure the oliguria will not respond to a fluid challenge. Management demands
accurate matching of input to output, monitoring of electrolytes and even dialysis.
 This is commonly the result of hypovolaemia. To restore, fluidbolus 250mL/30min is give and
reassessment of the patient. May need to reduce the dose in the elderly and those with a
history of heart disease. Check wether the output ahs increased and ascertain that the
patient is not overloaded with fluid as ti can cause acute heart failure esp in those with pre-
existing heart disease or elderly.
 Colloid solutions are used as they remain longer in the intravascular space due to their
high oncotic pressure
 Fluid overload requires the treatment with a diuretic  fruisemide (a non-potassium sparing
loop diuretic and venodilator)  this can be done IV or orally. The drug with relieve the
heart by reducing the preload through venodilation and the diuretic effect will peak in 30min
and lasts for 6hrs
 If after the first fluid challenge, there is nil result, try again and if after the second challenge,
seek help
 Renal causes
 Frusemide + mannitol
 Emergency dialysis if
 Severe hypovolaemia unresponsive to diuretics
 Intractable acidosis
 Severe hyperkalaemia
 Pericarditis secondary to uraemia
 Severe uremic sx or encephalopathy
 Call for help. May be out of scope for junior dr
 Post-renal cause
 Place a catheter
 If flow starts immediately, then suspect obstruction
 If catheter already present, replace or irrigate/flush it as it could be obstructed
 Urologist consult
 Seek help in the following cases
 Suspecting haemorrhage
 Sepsis
 Shock
 Dx unclear
 Tx failure
 Patients with ascities
 Patients with pre-exisitng renal disease
 Suspecting acute renal disease
 Dialysis
 Pulmonary oedema

Ologuria and ARF systemic complications

 Infections of Urinary tract and lungs can be due to uremia
 Up to 70% of pts with ARF
 Anaemia
 Renal production of EPO
 3rd space disease
 Salt and water retention esp in pre-renal failure
 Pulmonary oedema
 Pleural effusion
 Ascities
 Hypocalcaemia
 Decrease excretion of phosphate leading to impaired GI Ca absorption
 Hyperkalaemia
 Decrease GFR and tubular secretion
 Malaise
 Nausea
 Muscle weakness
 Cardiac emergency
 Metabolic acidosis with increased anion gap
 Decrease excretion of acids and tubular reabsorption of bicarbonate leading to metabolic
acidosis and high anion gap
 Hypotension
 Kussmaul’s respiration

 x
This is a common problem seen on overtime.

First step is to ensure that it is true oliguria. That is, make sure that the indwelling urinary
catheter isn’t blocked or that there isn’t a post-operative urinary obstruction/retention (by
physical examination of the abdomen and a ward bladder scan optimally).

“Low urine output” in a non-catheterised patient in the middle of the night is usually a
furphy. My “urine output” is usually zero as well. Any patient with suspected oliguria needs
an indwelling catheter and hourly urine output measurements.

Secondly, ensure that the patient doesn’t have pre-existing renal failure to explain the oliguria
(look up the pre-op UECs).

Any urine output below 30 mL/h should be considered acute renal failure, but that doesn’t mean
that a urine output of 40 mL/h is “okay”. Optimally, you should aim for a urine output of at least
1 mL/kg/hr.

Your target post-operative urine output is > 1 mL/kg/hr

Assuming the patient has previously normal renal function, oliguria indicates significant
dehydration/fluid deficit.

A good “formulative” approach to this is:

Algorithm for post-operative oliguria

Fluid choice: 0.9% NaCl (normal saline), 1 L bags.

 Step 1: 500 mL bolus, then the remainder of the bag at 500 mL/h (q2h), then
 Step 2: A bag at 250 mL/h (q4h), then
 Step 3: A bag at 166 mL/h (q6h), then
  Proceed onto usual maintenance fluids.

DO

 Review fluid hydration at the completion of each “bag” of fluid;

 if inadequate response, either repeat the current “step”, or go back a step;
 be mindful of spurious causes of oliguria;
 be mindful of possible acute tubular necrosis if poor responses to fluid challenges;
 be mindful of possible occult fluid losses (e.g., third space losses and hidden post-
operative bleeding);
 check electrolytes, urea and creatinine the next morning.

If on review, the patient has signs of shock, then proceed immediately to fluid resuscitation.

 Otherwise, first give a bolus (i.e., as quickly as it will go) of 500 mL of 0.9% NaCl (normal
saline) and then increase the rate of fluids after the bolus to 500 mL/hr (i.e., q2h).
 Review in an hour (which should be when the 1 litre bag of saline finishes). There should,
hopefully be an increase in the urine output in the past hour.
 If not, give another bolus and continue the rate of fluids at 500 mL/hr.

If there is still no improvement in the urine output after that (i.e., you have given 2 litres of fluids
over two hours), this usually means that the patient has gone into acute renal failure (i.e., acute
tubular necrosis) and you cannot use the urine output to necessarily judge the adequacy of your
intravenous fluid therapy (need to access the patient’s fluid status more generally and look at the
JVP to ensure you aren’t overloading the patient).

If there is a good response to the first or second bolus of fluid, then the next bag of fluid should
be 0.9% NaCl at 250 mL/h (i.e., q4h).

 The bag after that should be Normal Saline at 166 mL/h (or q6h).
 The bag after that should be Normal Saline at 125 mL/h (or q8h) which should be back to
approximately maintenance.
In fluid resus

here is only “one” rule for both adults and children:

Normal saline :: 10-20 mL/kg bolus :: fast as you can

If someone is shocked and requires emergency fluid resucitation, your fluid of choice is 0.9%
NaCl or “normal saline”. Don’t fluff around with colloids or Hartmann’s solution – choose bog
standard saline.

For your average adult, round to the litre – so that would be giving either one or two bags of
saline stat. And “stat” means as fast as you can through a large bore IV cannula (by gravity or by
hand pump). The infusion machines (“Baxters”) only go as fast as 1L per hour. You don’t have an
hour. You should be able to get a litre in over a handful of minutes (should definitely be less than
10 minutes).

For children, you would probably aim more for a 20 mL/kg bolus rather than 10 mL/kg and you
wouldn’t round off. An 8 kg child should get a 160 mL bolus of saline. For the smaller volumes in
children, it is often possible to push it in directly with a few large (e.g., 50 mL) syringes by hand.

After two 20 mL/kg fluid boluses in children, or 2 litres of fluid in adults, if there is no or poor
response, you need to start transfusing blood / infusing inotropes, etc.
Oliguria is a sx of an underlying disorder so need to treat the disorder as if left untreated, it can lead
to acute renal failure ARF and its sequelae – hyperkalaemia, acidosis, fluid overload

Pre-renal – stems from the inadequate management of fluids peri-operatively

It is important to seek the underlying cause. Fi the patient is dehydrated then ask why? Did it occur
due to poor perioperative fluid management, vomiting or diarrhoea. Is there haematuria
In the post-operative epriods, later on, sepsis can also be the cause of hypovolaemia due to fluid
shift from the intravascular space into the interstitium through leaky capillaries
Acute heart failure leading to poor CO and perfusion of the kidneys  why has the pt developed
meart failure? Is it due to iatrogenic fluid overload, cardiac arrhythmia/AF or ischaemia
Drugs  ACEI can cause pre-renal oliguria, nephrotoxic drugs leading to intrinsic renal disease

Box 1: Causes of postoperative oliguria

 Prerenal causes
 Hypovolaemia (most common cause)
 Dehydration, typically because of inadequate perioperative fluid management
 Fluid depletion-for example, caused by vomiting, losses from nasogastric tube,
diarrhoea, high output stoma, diuretic therapy, heat, fever, burns
 Sepsis (usually after the second day)
 Haemorrhage from operative site
 Acute heart failure
 Cardiac event including myocardial infarction and arrhythmia (especially atrial
fibrillation)
 Iatrogenic fluid overload
 Renal hypoperfusion
 Drugs interfering with mechanisms that maintain renal perfusion (non-steroidal anti-
inflammatory drugs, angiotensin converting enzyme inhibitors, angiotensin II receptor
antagonists, cyclo-oxygenase 2 inhibitors)
 Hepatorenal syndrome
 Oedema states
 Acute heart failure (see also above)
 Nephrotic syndrome
 Decompensated liver disease
Renal causes

 Intrinsic renal disease

 Following prolonged period of hypovolaemia
 Nephrotoxic drugs (for example, gentamicin)
 Acute exacerbation of pre-existing renal disease
Postrenal causes

 Urinary tract outflow obstruction

 Obstructed catheter
 Benign prostatic hypertrophy
Assessment
 Hx
 Is there evidence of pre-existing heart or renal disease
 Has the patient been taking corticosteroids prior to the surgery
 Have they been stopped perioperatively, which may aggravate hypotension
 Is the patient alert and orientated  drowsiness and confusion can indicate shock
 Is the patient using anti-hypertensives  this can contribute to renal hypoperfusion OR
NSAIDS
 How much fluid has been administered intraoperatively
 Has an epidural analgesia been given  risk of hypotension
 Exam
 Determine that the patient is haemodynamically stable
 If the patient is in shock, resuscitate
 Determine the patient’s circulatory volume i.e. is the patient hypovolaemic, euvolaemic or
overloaded with fluids. NOTE that many of the signs overlap and so interpre the signs
together
 In patients where this is difficult e.g. ascities; central venous pressure through a central
line is necessary to determine this. The CVP can be measured either manually or
electronically
 It is the change in CVP after a fluid challenge that provides the information required to
guide management
 If after a fluid challenge, CVP transiently rises and then falls or does not rise at all,
hypovolaemia or ongoing fluid loss/haemorrhage
 If the CVP rises and remains high, circulation is filled
 Determine an underlying dx that explains the drop in urine output. NOTE that haemorrhagic
shock may have normal haemoglobin in the initial stages and only falls once tissue fluid has
shifted into the circulation, diluting the blood
 Signs of shock can be masked by B Blockers or epidural anaesthesia


 D

Key signs of volume

Sx Hypovolaemia Hypovolaemia Euvolaemia Fluid overload
due to due to sepsis (normal fluid)
dehydration
Temp of hands Cold Warm Normal Cold
Cap refill Delayed Delayed Normal Delayed
Skin tugour Poor ?normal Normal Normal
Tongue Dry ?moist Moist Moist
JVP Low/not visible Low/not visible Not raised Raised
Crackles on No No unless focus No Yes
auscultation of chest
infection
Peripheral No No No Yes
oedema