Central Diabetes Insipidus

OVERVIEW

Diabetes insipidus (DI) is a condition caused by loss of the effect of antidiuretic hormone on the collecting ducts of the kidneys, resulting in loss of free water.

  • diabetes insipidus can be central or nephrogenic
  • This article will focus on CDI

PATHOPHYSIOLOGY

Normal physiology

  • ADH is produced in the hypothalamus and travels along nerve fibers to the posterior pituitary, where it is stored and released
  • Increased plasma osmolality stimulates release of ADH
  • ADH promotes reabsorption of water in the collecting duct of nephrons via translocation of aquaporins (water channels) to the plasma membrane from internal sites within the cells

Diabetes insipidus

  • central DI (CDI) results from causes that impair the synthesis, transport, or release of ADH
  • nephrogenic DI (NDI) results from receptor, or downstream, unrepsonsiveness to circulating ADH
  • loss of ADH effect results in polyuria, dehydration, hypernatremia and a hyperosmolar state

CAUSES OF CENTRAL DIABETES INSIPIDUS

Acquired

  • Surgery (transsphenoidal) – common
  • TBI – common
  • Idiopathic
  • Autoimmune
  • Tumours (suprasellar, lung, breast, lymphoma, leukaemia)
  • Hypoxic brain injury
  • Brain stem death
  • Profound hyponatraemia -> cerebral oedema
  • Radiotherapy
  • Inflammatory conditions – sickle cell, sarcoid, Wegener’s, histiocytosis X
  • Infections – Tb, abscess, encephalitis, meningitis
  • Vascular disease – CVA, SAH, Sheehan’s syndrome, pituitary apoplexy

Congenital

  • Autosomal dominant mutation in ADH production
  • Wolfram syndrome

DIAGNOSIS

Key findings

  • plasma hyperosmolality (can be mild in partial DI)
  • hypernatraemia (na >155 mM)
  • polyuria (>3L/24h)
  • urine osmolality < 200 mOsm/kg

Water deprivation test

  • rarely performed in the critical care setting
  • usually 4-18h water deprivation with serial urine and plasma osmolality until:
    — 5% loss of body weight
    — 2 urine samples with <30 mOsm/kg
  • then check ADH level
  • then give 1mcg DDAVP and check urine osmolality at 30 min and 60 min
  • results:
    — psychogenic polydipsia: urine osmolality > plasma osmolality; <10% increase in urine osmolality after ADH
    — CDI: urine osmolality < plasma osmolality; >50% increase in urine osmolality after ADH
    — NDI: urine osmolality < plasma osmolality; <50% increase in urine osmolality after ADH

Investigate for underlying cause

MANAGEMENT

(1) treat hypernatraemia
(2) address deficit in total body H2O (dehydration and hypovolaemia)
(3) supplement ADH
(4) consider associated anterior pituitary dysfunction
(5) treat underlying cause

  • manage in a critical care environment
  • measure Na+ frequently

Hypernatraemia

  • replacement of the previous hours urine output with an appropriate fluid
  • avoid a fall in Na+ concentration by more than 0.5mml/hr

Dehydration and Hypovolaemia

  • use isotonic saline
  • if hypernatraemia is > 155 -> then also use hypertonic saline to reduce the rate of reduction

ADH supplementation

  • if patient is euvolaemic -> DDAVP (V2 receptor agonist) 1-4mcg/day IV/IM/SC/IN
  • can infuse and titrate against urine output

PROGNOSIS

Post-traumatic diabetes insipidis is associated with:

  • more severe trauma
  • cerebral edema
  • lower GCS scores
  • higher mortality rate
    • 57-69% overall
    • 86-90% if early-onset (<3 days after injury)
  • brain death (DI is present in ~80% of brain dead TBI patients)
  • hypernatraemia correlates with higher mortality (e.g. Na >160 mmol/L)

References and Links

Journals

  • Di Iorgi N, Napoli F, Allegri AE, Olivieri I, Bertelli E, Gallizia A, Rossi A, Maghnie M. Diabetes insipidus–diagnosis and management. Horm Res Paediatr. 2012;77(2):69-84. PMID: 22433947
  • Makaryus AN, McFarlane SI. Diabetes insipidus: diagnosis and treatment of a complex disease. Cleve Clin J Med. 2006 Jan;73(1):65-71. PMID: 16444918

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. 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 two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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