Skip to content
  • Home
  • JMO Companion App
YouTube Facebook LinkedIn
YouTube Facebook LinkedIn
  • JMO Companion App
Teaching for ImpactTeaching for Impact
  • Programs
    • VCE Program (RESET)
    • Medicine Program
      • Pre-Clinical Lecture Series
      • OSCE Video Series
      • A3 Tutorials
      • Virtual Ward Round Series
      • Clinical Skills Booklet
    • HSC Program
  • Discover
    • Volunteer
Volunteer
Teaching for ImpactTeaching for Impact
Popular Search heart failurehypertensionpneumothoraxhyperkalaemiahypotension

Skills

  • Approach to MET call
  • Indwelling catheter
  • Basic Life Support (BLS) – Adults

Cardiology

  • Acute coronary syndrome
  • Ventricular tachycardia
  • Supraventricular tachycardia
  • Bradycardia
  • Chest pain
  • Heart failure
  • Hypertension

Endocrinology

  • Hypophosphataemia
  • Hypoglycaemia
  • Diabetic ketoacidosis and hyperosmolar hyperglycaemic state
  • Vitamin D deficiency
  • Hypernatremia
  • Hypokalaemia
  • Hyperkalaemia
  • Hypercalcaemia
  • Hyperglycaemia
  • Hypocalcaemia

Urology

  • Haematuria

Palliative care

  • End-of-Life Care

Neurology

  • Acute drop in GCS
  • Vertigo
  • Headache

Respiratory

  • Pneumonia
  • COPD exacerbation
  • Hypoxia
  • Asthma exacerbation
  • Pneumothorax

Geriatrics

  • Falls

Infectious diseases

  • Urinary tract infection
  • Febrile neutropenia
  • Positive blood cultures
  • Cellulitis

Emergency

  • Epistaxis

Gastroenterology

  • Abdominal pain
  • Refeeding syndrome
  • Nausea and vomiting

Haematology

  • Oral Anticoagulants Dosing 

Nephrology

  • Oliguria

General medicine

  • Hypotension
  • Alcohol withdrawal
  • Fluids
  • Delirium
  • Home
  • jmocompanion
  • Nephrology
  • Oliguria

Oliguria

Table of Contents
  • Overview
  • Triage
  • Causes
  • Diagnosis
  • Approach
    • History
    • Exam
  • Investigations
  • Management
  • Appendix A: Common nephrotoxins and nephrotoxic events

Overview #

  • Oliguria is often the first sign of a developing kidney injury
  • Oliguria is not always pathological, but urine output <0.5mls/kg/hr for ≥ 2 consecutive hours warrants review
  • New hypotension plus oliguria may be the first sign of shock ([link to shock guideline?])
  • Causes can be divided into pre-renal, renal and post renal: Pre-renal accounts for ~90% of inpatient AKI, but always consider obstruction (post-renal) and renal causes before prescribing a fluid bolus
  • There are 4 urgent complications for AKI : refractory fluid overload, acidosis, hyperkalaemia, and uraemic complications (encephalopathy, serositis, etc.)

Triage #

Attend within one hour

Causes #

Pre-renal – ie: hypoperfused kidney(s)

  • Hypovolaemia – intravascular fluid depletion (eg: GI losses, prolonged fasting, haemorrhage)
  • Low output states – Heart failure
  • Focal reduction in renal perfusion – Decompensated liver failure, renal artery stenosis, abdominal compartment syndrome

Renal 

  • The vessels
    • Loss of autoregulation of afferent/efferent arterioles from NSAIDs or ACEi
  • The glomerulus
    • Glomerulnephridities – a group of conditions which can be categorised, based on presentation, into nephrotic and nephritic syndromes
  • The tubules
    • Acute tubular necrosis (longstanding pre-renal failure)
    • Rhadbomyolysis
    • Tumour lysis syndrome
  • The interstitium
    • Acute interstitial nephritis
      • Diagnostic triad = fever, skin rash, eosinophilia
      • Usually drug related and takes several weeks of exposure to develop – suspect PPI, NSAIDs, sulphonamides, b-lactams, cephalosporins, fluroquinolones, isoniazid, rifampicin. 
      • Less commonly due to tumour lysis syndrome, Sjogrens, SLE or RA
    • Thrombotic thrombocytopenic purpura
      • Diagnostic pentad = AKI, anaemia, thrombocytopaenia, fever and neurological dysfunction

Post renal

  • Blocked IDC
  • Kidney stones
  • Prostatic hyperplasia 
  • Urinary retention, which can be caused by:
    • Drugs (especially anticholinergics)
    • Constipation
    • Haematuria with clot
  • Retroperitoneal pathology

Diagnosis #

Oliguria is often the first sign of developing kidney injury.

Take seriously a urine output of

  • <0.5mls/kg/hr for more than two consecutive hours
  • <400mls/day

Approach #

Review the chart, check:

  • Fluid balance over the last few days (daily weights even better)
  • Renal function – establish baseline and current trend
  • Any nephrotoxins or on the drug chart (Appendix A)
  • Any nephrotoxic insults in recent days (Appendix A)
  • Current vital signs
History #

Check for:

  • Abdominal pain
  • Macroscopic haematuria or abnormal urinalysis
  • Obstructive symptoms – “lower urinary tract symptoms” (LUTS)
    • Difficulty starting or maintaining stream
    • Nocturnal voiding
  • Previous kidney stones
  • Infective symptoms
    • Dysuria
    • Frequency
    • Urgency
Exam #
  • Check if there is a catheter in situ – if so, could it be blocked?
  • Is the bladder palpable? If so, it’s grossly enlarged
  • Note what the urine looks like, specifically:
    • Any haematuria, and if present if there are clots
    • If it froths when you shake the IDC box (sign of proteinuria)
    • Dark and concentrated or clear/straw coloured
  • Fluid state (are they grossly dehydrated or fluid overloaded?)
  • Any signs of complications of renal failure
    • Confusion, asterixis
    • Kussmaul breathing (metabolic acidosis)
    • Pericardial rub (uraemic pericarditis)

Investigations #

All patients

InvestigationSignificance
Bladder scanExclude urinary retention/blocked catheter
UECs

Unless the cause is clearly pre-renal and responds quickly to a bolus of IV fluid also arrange:

Urine dipstick Bedside test for infection and proteinuria
Urine MCS and protein:creatinine ratioFormal assessment for infection and proteinuria
Renal tract ultrasoundExclude a post renal cause (ie: obstruction)If renal artery stenosis is suspected then specifically request a doppler study

To workup an intrarenal cause, particularly if abnormal proteinuria or haematuria detected on dipstick, consider the below (in consultation with the renal team)

#HIV/HCV/HBVBlood borne virus screen
#ANA/ENA/dsDNA/ANCA/anti GBM/Anti-strep Ab/PLA2R/C3/C4Vasculitis screen
CKExclude rhabdomyolysis

For patients in frank renal failure

ECGExclude features of hyperkalaemia
VBGCheck pH and potassium
CXRCheck for pulmonary oedema

Management #

All patients

  • Strict fluid balance chart (consider IDC if not already in situ)
  • Daily weights (often more accurate than fluid balance chart)
  • Daily UECs
  • Withhold nephrotoxic drugs (if possible)
  • Check drug chart for anything that needs to be dose reduced based on current renal function
    • Especially antibiotics, clexane, NOACs, insulin and blood sugar lowering medications, digoxin
    • If significant AKI strongly consider ceasing any potassium supplements
  • Consider if there is an indication for dialysis (and if so urgently refer renal +/- ICU)
    • Acidaemia (pH <7.2)
    • Hyperkalaemia (K>6 despite medical management, see here)
    • Intoxication with dialysable drug
    • Pulmonary oedema (see here)
    • Uraemic encephalopathy or uraemic pericarditis (or, if urea >40 dialysis should at least be considered)

Treatment dependent on cause

  • Pre-renal
    • Treat cause if identified
    • If clinically hypovolemic bolus IV crystalloid and review. Be mindful of cardiac function, avoid pulmonary oedema
    • If clinically overloaded the problem is more challenging. Discuss with senior.
  • Renal
    • investigations as above
    • refer renal team
  • Post renal
    • Relieve obstruction
      • Most often this involves inserting an IDC, or replacing one that’s blocked
      • If obstruction higher in urinary tract (eg: vesicoureteric junction) will need urology consult
    • Monitor for post-obstruction diuresis (suspect after obstruction is relieved if urine output >200ml/hour for >2 hours or >3litres in 24 hours)
    • If post obstructive diuresis does occur
      • Start strict fluid balance chart
      • Commence normal saline at 50-80% of the urine output/hour
      • Check electrolytes BD – TDS and replace electrolytes 

Appendix A: Common nephrotoxins and nephrotoxic events #

  • Surgery which involved clamping arterial supply
  • Things that cause dehydration
    • Vomiting/diarrhoea/polyuria
  • Things that cause rhabdomyolysis
    • trauma/crush injury/immobilization
  • Drugs
    • ACEi/ARBs
    •  NSAIDs
    • Diuretics
    • PPIs (AIN)
    • Gentamicin/vanocymin (tubular toxins)
    • Penicillins/cephalosporins/rifampicin (AIN)
    • IV Contrast scans
  • Angiogram – cholesterol emboli
  • Hypercalcaemia –tubular toxin
  • Contributors

  • Reviewing Consultant/Senior Registrar

Dr Scott Santinon

Dr Euzebiusz Jamrozik

What are your Feelings
Share This Article :
  • Facebook
  • Twitter
  • LinkedIn
  • Pinterest
Updated on March 27, 2023
Table of Contents
  • Overview
  • Triage
  • Causes
  • Diagnosis
  • Approach
    • History
    • Exam
  • Investigations
  • Management
  • Appendix A: Common nephrotoxins and nephrotoxic events

Teaching for Impact

Our mission as a group of young leaders is to create positive and meaningful change in the community through education. We offer a variety of initiatives that empower different sectors of society to realize their full potential and use their skills, knowledge, and experience to enhance the lives of those in their surroundings.

Find us on socials

YouTube Facebook Twitter Instagram
  • Privacy Policy
  • Cookie Policy
  • Terms and conditions

Made with ♥ for the community