Hyponatraemia
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Duggal, A.K et al (2006) “Clinical Approach to Altered Serum Sodium Levels” JIACM 7(2):91103
UptoDate
- common problem in ICU (30% of patients have a Na < 134mmol/L)
- independent predictor of mortality in ICU
- goals = to determine:
(1)
(2)
(3)
(4)
severity
type
treat cause
prevent complications
SEVERITY
Na+ < 135mmol/L
Mild 125-134
Moderate 120-124
Severe <120
TYPES and CAUSE
Hypoosmolar/Hypotonic -> hypovolaemic, euvolaemic and hypervolaemic
Isoosmolar
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
Jeremy Fernando (2011)
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 (PAM tHe COD)
Pulmonary
ADH secretion (ectopic)
Malignancy
Hormone deficiency
CNS disease
Others
Drugs
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.
Jeremy Fernando (2011)
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+
sodium deficit = 0.6 x weight in kg x [Na desired - Na measured]
Jeremy Fernando (2011)
MANAGEMENT
-
treat cause
ideally correct slowly to avoid central pontine myelinolysis
quantify duration, severity and type
treatment is dependent on cause
(1)
(2)
(3)
(4)
(5)
fluid restriction (< 800mL/day)
diuretics
isotonic saline (in true volume depletion)
oral Na+ tablets
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!)
Jeremy Fernando (2011)
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
Jeremy Fernando (2011)