Hyponatraemia

OVERVIEW

  • common problem in ICU (30% of patients have a Na < 134mmol/L)
  • independent predictor of mortality in ICU
  • goals = to determine:
  1. severity
  2. type
  3. treat cause
  4. prevent complications

SEVERITY

Na+ < 135mmol/L

  • Mild 125-134
  • Moderate 120-124
  • Severe <120

TYPES AND CAUSES

  • Hypoosmolar/Hypotonic
    • -> hypovolaemic, euvolaemic and hypervolaemic
  • Iso-osmolar
  • Hypertonic

Hypotonic/Hypoosmolar

  • causes = solute depletion or solute dilution

Hypovolaemic

  • loss of H2O and Na from the ECF -> increased ADH secretion -> decreased free H2O excretion and H2O retention -> hyponatraemia
  • renal or extra-renal causes

RENAL LOSS

  • diuretics
  • osmotic diuresis (glucose, mannitol)
  • bicarbonaturia (RTA)
  • salt wasting nephropathy
  • mineralocorticoids deficiencies
  • ketones

NON-RENAL LOSS

  • upper GI: vomiting
  • middle GI: pancreatitis, bowel obstruction
  • lower GI: diarrhoea, bowel preparation
  • other losses: sweat, bleeding
  • the way to sort out whether it is a renal or extra-renal source = to do a urinary Na+
  • if urinary Na+ < 10mmoL/L -> extra-renal (as kidney appropriately attempting to hold onto Na+)
  • if urinary Na+ > 20mmol/L -> renal (as if clinically hypovolaemic then this is an inappropriate response)

Euvolaemic

  • causes = SIADH (most common), psychogenic polydipsia, hypotonic IVF therapy, adrenal insufficiency, hypothyroidism
  • any disease state causing hypoosmolality can present with a normal state of hydration
  • clinical examination of volume status is not sensitive
  • more sensitive = a normal or low urea and an elevated urinary Na+

See SIADH document for further information

Causes of SIADH (=MAD CHOP)

  • Malignancy
  • ADH secretion (ectopic)
  • Drugs (e.g. SSRIs, ecstasy)
  • CNS disease
  • Hormone deficiency (hypothyroidism, adrenal insufficiency)
  • Others
  • Pulmonary

Hypervolaemic

  • increase in total body Na+ and H2O -> however, total body H2O is out of proportion to Na+
  • clinically evident oedema or ascites
  • causes: CHF, cirrhosis, nephrotic syndrome, hypothyroidism, pregnancy, TURP/hysteroscopy syndrome

Isotonic

  • known as “pseudohyponatraemia”
  • plasma osmolality can be measured directly in the laboratory using a osmometer or by the formula: calculated osmolarity = (2xNa+) + glucose + urea
  • serum is made up of 93% H2O and 7% non-aqueous factors including lipids and proteins
  • normally the nonaqueous components do not effect the tonicity but in states of marked hyperproteinaemia or hyperlipidaemia (elevated chylomicrons or triglycerides) -> this ratio is changed artifactually decreasing the apparent concentration of Na+ in serum.

Hypertonic

  • translocational hyponatraemia
  • osmotically active particles in the plasma induces movement of H2O from ICF -> ECF -> decreasing serum Na+ even though the serum osmolality remains elevated.
  • agents that cause this: glucose, mannitol, sorbitol, radiocontrast
  • for each 1mmol/L rise in blood glucose the serum sodium will decrease by 0.3mmol/L

*** Advanced renal disease = an important cause of a normal or high serum osmolality

  • hyponatraemia from the inability to excrete H2O -> lowers osmolality but because of high urea this acts to normalise osmolality or can make it high.
  •  however, urea is an ineffective osmole (as it freely crosses cell membranes) -> therefore does not cause H2O to moved out of cells.
  • you need to correct serum osmolality for the effect of urea: Corrected serum osmolality = measure osmolality – [urea]

HISTORY

  • speed of onset more important than level
  • most patients won’t be symptomatic until Na+ < 125mmol/L
  • fluid intake/output
  • nausea
  • vomiting
  • neuropsychiatric symptoms
  • muscular weakness
  • headache
  • lethargy
  • psychosis
  • raised ICP
  • seizures
  • coma
  • medications!
  • ROS to find precipitant and organ dysfunction
  • co-morbidities: adrenal disease, liver disease

EXAMINATION

  • cause!
  • volume status
  • neurological complications (increased ICP, lateralizing signs)

INVESTIGATIONS

  • diagnostic
  • U+E (Na+, glucose, renal function)
  • plasma osmolality
  • plasma proteins and lipids
  • urinary Na+

MANAGEMENT

  • treat cause
  • ideally correct slowly to avoid central pontine myelinolysis
  • quantify duration, severity and type
  • treatment is dependent on cause

(1) fluid restriction (< 800mL/day)
(2) diuretics
(3) isotonic saline (in true volume depletion)
(4) oral Na+ tablets
(5) hypertonic saline (3%):

-> rapid reversal – 100mL (raises Na+ by 2-3mmol/L) Q 10 min until seizures stops
-> less rapid – 1mL/kg/hr of LBW

  • can use desmopressin or dextrose if inadvertent rapid correction takes place

Acute (<48hrs) and symptomatic

  • seizing and coma
  • raise by 1-5mmol/L/hr until symptoms resolve or Na+ 125-130mmol/L
  • hypertonic saline (3%) 1-2ml/kg/hr
  • frusemide 20mg IV

Chronic symptomatic (>48 hrs or unknown duration)

  • calculate Na+ deficit
  • correct Na+ by 10mmol/L/day
  • frusemide 20mg IV
  • N/S
  • fluid restrict
  • repeat Na+ every 2 hours
  • high risk patients = young premenopausal woman

Asymptomatic from SIADH

  • fluid restrict
  • frusemide 20-40mg/day
  • NaCl tablets 3-18g/day
  • urea 30g/day
  • demclocycline 600-1200mg/day
  • current trials underway looking @ AVP V2 receptor antagonists

NORMAL RANGES

  • Serum osmolality: 272-295mOsm/kg water (panic values = 240 and 320!)
  • Urine osmolality: from 50-1400mOsm/kg water (average 500-800) – after an overnight fast urine osmolality should be 3 times the plasma osmolality
  • Urinary Na+ – 15 to 250 mmol/L

CALCULATIONS

  • Use calculators at
  • sodium deficit = TBW x [Na desired – Na measured]
  • rate of infusion (mL/hr) = Na requirement (mmol) x 1000 / infusate Na (mmol/L) x time (hours)
  • Androgue formula: Change in serum Na+ = (infusate Na + infusate K) – serum Na /TBW + 1

Total body water

  • Children = 0.6 x weight
  • Women =0.5 x weight
  • Men = 0.6 x weight
  • Elderly Women = 0.45 x weight
  • Elderly Men = 0.5 x weight

Sodium content of different fluids (i.e. infusate Na in mmol/L)

  • 5% NaCl = 855
  • 3% NaCl = 513
  • 0.9% NaCl (NS) = 154
  • Lactate Ringer’s = 130
  • 0.45% NaCl (½ NS) = 77
  • 0.2% NaCl (¼ NS) = 34
  • 5%Dextrose in water (D5W) = 0

References and Links

Journal articles

  • Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000 May 25;342(21):1581-9.Review. [pubmed] [article]
  • Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. European journal of endocrinology. 2014; 170(3):G1-47. [pubmed] [article]

FOAM and web resources


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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