SODIUM DISORDERS

Hyponatremia
Common electrolyte disorder in the inpatient setting
Occurs in 15-30% of hospitalised patients
Defined as serum Na <135mmol/L

Clinically important because

1) Associated with increased mortality in both the

ambulatory and inpatient setting

2) Confers a poorer prognosis in a range of underlying
diseases including cirrhosis, pulmonary HTN, MI, CKD,
hip fractures and PE
3) Rapid correction can cause severe neurological deficits
and death
AJM 2013

Regulation of body water

Disturbances in serum Na are generally due to changes

in the bodys water balance, not sodium, i.e. changes in

plasma osmolality.
osmolality sensed by the osmo-receptors in the
hypothalamus thirst & release of ADH water
reabsorption from renal collecting ducts.
Non-osmotic stimuli (hypovolaemia, stress, nausea) can
also cause ADH release (even if serum osmolality is
normal or low)

Hyponatremia
Approach:

(1) Measure plasma osmolality

(2) Assess extracellular volume

Classification according to plasma

osmolality
1. Isotonic hyponatremia (280-285mOsm/kg):
*Pseudohyponatremia ; hyperlipidemia or
hyperproteinemia results in low measured Na
concentration (but osmolality is normal)
(rare lab artefact)
2. Hypertonic hyponatremia (>285mOsm/Kg):
excess of another effective osmole (glucose,
mannitol/sorbitol) that draws water intravenously
3. Hypotonic hyponatremia (<280mOsm/kg):
most common scenario
true water excess relative to Na ( salt loss).

Serum osmolality and sodium

Serum Osm = 2x [Na+] + glucose + urea
(units all in mmol/L)
Corrected Na+ = Measured Na + 0.3 x (serum glucose
5.5) mmol/L

AJM 2013

Hyponatremia
Approach:

(1) Measure plasma osmolality

(2) Assess extracellular volume

Volume status
Assess volume status (extracellular fluid volume)
Hypotonic hyponatremia has 3 main etiologies:
Hypovolemic both H2O and Na decreased (H2O < Na)
Consider obvious losses from diarrhea, vomiting, dehydration,

malnutrition/poor oral intake, diuretics etc

Euvolemic H2O increased and Na stable
Consider SIADH, drugs, thyroid disease, glucocorticoid deficiency

Hypervolemic H2O increased and Na increased (H2O > Na)

Consider CHF, cirrhosis, renal failure

Measurement of urinary Na+ will help in differentiating the above

processes

serum osm (measured)

normal
measure lipids, proteins

volume expanded
CHF
Cirrhosis
nephrotic

low (<280)
Assess ECF Clinically

Volume Depleted
adrenal insuff
extrarenal losses
renal salt wasting

High (>>280)
glucose
mannitol, sorbitol, glycine

Euvolemic
polydipsia
SIADH

Hypotonic hyponatremia

 85yo man admitted with 3/7 of nausea/vomiting/diarrhoea

and headache
Na+ on admission found to be 122, baseline unknown
PHX:

Hypertension
IHD
Dyslipidaemia
OA

 Medications:

Aspirin 100mg D
Perindopril 10mg D
Atorvastatin 40mg nocte
Panadol Osteo

No focal neurological deficits; clinically dry

CT Brain NAD
Serum osmolality is 266. Urine osmolality is 465. Urine Na+
is 8

Hypovolemic. Serum osmolality is 266. Urine osmolality is 465.

Urine Na+ is 8

Treatment
IV N/Saline

 72yo woman from nursing home admitted with increasing

falls and recent headstrike

Na+ 125
PHx:

Dementia
CCF
Recurrent UTIs
Ex-heavy smoker

 Medications:

Irbesartan HCT 300/12.5mg D

Aspirin 100mg D
Esomeprazole 20mg D
Simvastatin 80mg nocte
Clinically euvolemic

CTB: nil acute pathology

CXR: 5cm right hilar mass
Na 125, serum osmolality 270, urine osmolality 122, urine

Na+ 55

Euvolemic. Serum osmolality is 270. Urine osmolality is 122.

Urine Na+ is 55

Treatment
Cease exacerbating drug (ie. HCT)
Fluid restriction

Bronchoscopy and biopsy: bronchogenic carcinoma

Before diagnosis of SIADH must rule out drugs,

hypothyroidism and hypocortisolism (as they can mimic

SIADH)

SIADH
Causes:
CNS: neoplasms, bleed, encephalitis/meningitis,

sarcoidosis, pituitary surgery, nausea

Drugs: SSRI, carbamazepine, haloperidol, amitriptyline,
bromocriptine, MDMA etc
Pulmonary disease: pneumonia, TB, ARDS, malignancy
Ectopic ADH: carcinomas (small cell lung ca),
pancreatic or duodenal ca, thymic ca

 55F presents to ED following witnessed seizure with

confusion and drowsiness

Na+ 108
PHx:

Chronic ETOH abuse (6L wine/day)

Hepatitis C
Anxiety and depression

 Medications:

Recently commenced on escitalopram by LMO for

depression
CTB: nil acute pathology

Multifactorial hyponatremia
Decreased solute intake in the setting of ETOH abuse

(beer potomania, tea and toast diet)

SIADH secondary to escitalopram

Treatment
Hyponatremia with neurological symptoms is a medical
emergency
Bolus of 100ml to 150ml of 3% hypertonic saline
Monitor hourly serum Na and aim for target Na of
120mmol/L
Indications for hypertonic saline:
- Severe symptomatic hyponatremia: seizures, altered
conscious state

Rate of Correction
The rate of sodium correction should be 6 to 12 mmol/L in
the first 24hrs and 18mmol/L or less in 48hrs
High risk of osmotic demyelination:
Serum sodium concentration <105mmol/L
Hypokalemia
Alcoholism
Malnutrition
Advanced liver disease

NEJM 2015

Vaptans
Vasopressin receptor antagonists, eg tolvaptan, have

been approved for treatment of hypervolemic or

euvolemic hyponatremia
Blocks action of endogenous ADH thereby increasing
water excretion whilst sparing solute loss (unlike
traditional diuretics such as frusemide)

JCEM 2013

Vaptans

Vaptans not currently on PBS for treatment of hyponatremia in

Australia
Due to cost and concerns regarding controlling rate of rise of serum
Na and hence increased risk of osmotic demyelination
JCEM 2013

Answer C

Hypernatremia

Diabetes Insipidus
Polyuria: > 3 L/d

Polydipsia: > 3.5 L/d

Ddx
Diabetes mellitus
Hypercalcaemia
Solute diuresis:
Volume expansion 2 saline loading
High-protein feeds (urea as osmotic agent)

Diabetes insipidus:
Central (CDI)
Nephrogenic (NDI)

Primary (psychogenic) polydipsia

Diabetes Insipidus DDx

Central (CDI)
Idiopathic
autoimmune

Neurosurgery, head trauma

Cerebral hypoperfusion
Tumor
Craniopharyngioma, pituitary

adenoma, suprasellar
meningioma, pineal gland,
metastasis
Infiltration
Fe, Sarcoid, Histiocytosis

Nephrogenic (NDI)
Genetic due to defect in
vasopressin or aquaporin
gene
Tubules not responsive to
vasopressin:
- Hypokalemia
- Hypercalcemia (2 to HPT in
particular)
- Renal disease: after ATN,
post-obstructive uropathy,
RAS, renal transplant,
amyloid, Sickle cell anemia
- Sjogrens syndrome
- Drugs:
Lithium, 20% of chronic users
amphotericin, colchicine

What is appropriate urine concentration?

1)
2)
3)
4)

Complete DI
Defective osmoreceptor, normal ADH release to ECFv contraction
High-set osmoreceptor: ADH release is sluggish/delayed
ADH release at normal Posm but subnormal in amount

Diabetes Insipidus
Healthy out-patients
DI with intact thirst or access to water
High-normal serum sodium (142-145 mmol/L)
Polydipsia (crave cold fluids)
Polyuria, Nocturia sleep disturbance

1 Psychogenic Polydipsia
Low-normal serum sodium (135-137 mmol/L)
Middle-aged women
Psychiatric illness, phenothiazine (dry mouth)

Diabetes Insipidus
Intact thirst & access to water
Hi-normal serum sodium (142-145 mEq/L)
Polydipsia (crave cold fluids)
Polyuria, nocturia sleep disturbance
1 treatment is DDAVP and drink to thirst
Impaired thirst or access to water:
Hypernatremia
Insufficiently concentrated urine
1 treatment is fixed free water replacement and
DDAVP

1 Polydipsia

Water Deprivation Test

Stop water intake for 2-3h prior to coming in
Continue to withhold water & monitor:

Urine volume, UOSM q1h

Serum Na, OSM q2h
If serum osmolality/Na+ do not rise above normal ranges & urine

osmolality reaches 600mOsm/kg 1 Polydipsia

If serum osmolality reaches 295-300 mOsm/kg & UOSM doesnt
Diabetes Insipidus established
Give DDAVP 10 mcg IN and monitor for further 3 hrs
Central DI: UOSM by 100-800% (complete CDI), by 1550% (partial CDI) with absolute UOSM > 345mOsm/kg
Nephrogenic DI: UOSM by up to < 9%, sometimes as
high as 45% but absolute UOSM always < isotonic (290
mOsm/kg)