Polyuria and Traumatic Brain Injury


  • polyuria following TBI is common
  • multiple causes, some of which imply a poor prognosis
  • Goal is to identify and treat the cause and any complications


Common and important causes

  • Alcohol induced diuresis
  • Osmotic diuresis (mannitol therapy)
  • Cerebral salt wasting
  • Diabetes insipidus
  • Hypertonic saline administration
  • Hypertensive diuresis (e.g. vasopressors to maintain CPP)
  • Appropriate response to fluid therapy or diuretics
  • Hyperglycaemia
  • Cold-induced hypothermia (either due to exposure or therapeutic hypothermia)
  • Co-existent renal disorder (e.g. polyuric phase of acute kidney injury)


  • recent osmotherapy (mannitol or hypertonic saline)
  • fluid balance and diuretic use
  • vasopressor use for CPP management
  • diabetes, hypertension, renal disease
  • ETOH
  • hypothermia


  • volume status
  • urine colour and volume
  • BP
  • temperature
  • evidence of DM, HTN or renal disease



  • Na+
  • osmolality
  • ETOH level
  • osmolar gap calculation


  • osmolality
  • Na+

Consider further investigation of renal disease if appropriate (e.g. UEC, ultrasound)


Alcohol induced diuresis

  • high ETOH level
    -> replace fluid loss

Osmotic diuresis (mannitol therapy)

  • high osmolar gap, osmolality and urinary osmolality
    -> monitor for hypovolaemia
    -> cease mannitol if osmolality > 320mosmol/kg
    -> replace electrolytes

Cerebral salt wasting (mimics SIADH biochemically but hypovolemic)

  • high urinary osmolality
  • low plasma Na+
  • plasma osmolality may be high or normal
    -> monitor for hypovolaemia, give normal saline

Diabetes insipidus

  • high Na+
  • low urinary osmolality (<350)
  • high plasma osmolality
    -> replace H2O or D5W
    -> DDAVP 0.5mcg

Hypertonic saline administration

  • high serum and urine Na+

Hypertensive diuresis

  • normal Na+ and osmolality
    -> monitor

Appropriate response to fluid therapy

  • normal Na+ and osmolality
    -> monitor


  • +/- low serum Na, metabolic alkalosis, high urine Na
    -> monitor, give fluids if needed;  consider acetazolamide


  • high glucose
  • glycosuria
    -> insulin

Cold-induce diuresis

  • hypothermia
    -> monitor, rewarm if appropriate, maintain euvolemia

CCC Neurocritical Care Series

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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