Diabetes Insipidus following TBI


  • Diabetes insipidus (DI) results from decreased secretion and action of anti-diuretic hormone (ADH)
  • ADH is produced in the hypothalamus and transported to the posterior pituitary gland
  • ADH is released into the circulation in response to thirst, increased plasma osmolarity and hypotension
  • It is a key hormone involved in water regulation and the defence of blood volume


In a head injured patient decreased production and secretion of ADH can result from:

  1. direct disruption of the hypothalamus or pituitary
  2. interruption of the blood supply to these parts of the brain
  3. increased ICP or oedema causing herniation of the brain and subsequent compression of the pituitary stalk or gland

Consequences of decreased ADH action

  • decreased H2O reabsorption in the collecting ducts of nephron
  • decreased Na+ reabsorption
  • increased K+ secretion
  • decreased GFR from relaxation of mesanglial cells in glomerulus
  • contraction of intravascular volume (dehydration and hypovolaemia)
  • polyuria
  • loss of tone in vascular tree causing hypotension
  • decreased aldosterone secretion
    -> decreased Na+ reabsorption, increased K+ loss
  • decreased angiotensin II
    -> vasodilation, decreased nordrenaline secretion from post-ganglionic sympathetic neurons, decreased thirst sensation, decreased ADH secretion


  • polyuria
  • high serum Na+
  • low serum K+
  • high plasma osmolality
  • high urinary Na+ (inappropriate)
  • high K+
  • low urine osmolality (inappropriate)
  • low plasma ADH level
  • worsening of biochemical markers with fluid restriction
  • improvement in biochemical markers and polyuria with desmopressin treatment
  • MRI to quantify anatomical integrity of hypothalamus and cerebral blood flow may be required to confirm diagnosis

References and Links

CCC 700 6

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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