Sodium Balance Flashcards
What is the commonest electrolyte abnormality in hospitalised patients?
- LOW Na (HYPOnatraemia/ HypoNa)
DEFINITION of Hyponatraemia
Serum sodium < 135mmol/L
normal range of sodium
- Normal range: 135-145mmol/L
Pathogenesis of Hyponatraemia
- Increased EXTRACELLULAR water
- (Get excess water due to increased ADH secretion
How does ADH work
- ADH is synthesised in the hypothalamus + released from posterior pituitary
- It acts on the distal tubules on kidneys to promote WATER RETENTION.
- It inserts Aquaporin 2 into the membrane to retain water + increase in extracellular water
more ADH =
MORE WATER REABSORPTION
which receptors does ADH work on
- Acts on V2 receptors on collecting duct = insertion of aquaporin 2
- Acts on V1 receptors on VSMCs >> vasoconstriction
ADH is stimulated by…. (2)
o HIGH serum osmolality: mediated hypothalamic Osmoreceptors
o LOW blood volume/ BP detected by baroreceptors in carotids, atria and aorta
• Osmolarity equation
2(Na+K) + urea + glucose
normal range: 275-295mOsmol/kg
**basc: cations+anions+ uncharged molecules**
increased ADH means
increased water retention = increased extracellular water = hyponatraemia
First Step in Clinical Assessment of a Hyponatraemic Patient
assessment of volume status: euvolaemic, hypo- or hypervolaemic
Clinical Signs of Hypovolaemia
- reduced skin turgor
- prolonged capillary refill
- dry mucous membranes
- hypotension (postural)
- Confusion/ drowsiness
- Reduced urine output
- LOW URINE Na+ (< 20)
MOST RELIABLE clinical sign of hypovolaemia
- LOW URINE Na+ (< 20)
**this is in the case of extra-renal losses**
**in renal losses eg if patient is on diurectics- they will have ah igh urine sodium regardless**
Clinical Signs of Hypervolaemia
- raised JVP
- ascites
- pulmonary oedema: bibasal crackles on chest examination
- peripheral oedema
hypovalaemic causes of hyponatraemia
renal causes:
- thiazide diuretics
- salt losing nephropathy
- salt wasting syndromes (post-operative)
extra renal causes:
- vomiting, diarrhoea
- burns
mechanism
- loss of fluid –> low BP–> detected by baroreceptors–>ADH release–>water reabsorption–>dilution of extracellular fluid
euovalaemic causes of hyponatraemia (and what is the mechanism?)
adrenal insufficiency (addison’s disease)
SIADH
hypothyroidism
mechanism
- to begin with these patients are euvolaemic- they have no problem with their volume status or blood pressure
- for some reason (not sure exact) these conditions cause ADH to be released–>water reabsorption–>raises BP
- body doesn’t like this raised BP–>releases ANP–>natriuresis (loss of sodium + some fluid)–> this then normalises the volume status, but in the process they have lost some sodium
hypervolaemic causes of hyponatraemia and what is the mechanism?
cardiac failure
nephrotic syndrome /renal failure
cirrhosis
mechanism
- heart failure: pump failure –> low BP–> ADH release–> water reabsorption
- cirrhosis: high nitric oxide and other vasodilators (as the liver cannot break them down)–>fall in BP–>ADH release–>water reabsorption
- renal failure: kidneys aren’t functioning–>reduced water excretion–>more water retention–>hyponatraemia
is hypovalaemia same as dehydration
- Dehydration is JUST loss of water
- Hypovolaemia is loss of SALT AND WATER
hypovolaemic hyponatraemia: how to distinguish between renal vs non-renal losses ?
o Urine Na > 20- renal losses (e.g. diuretics, salt-wasting syndromes)
o Urine Na < 20- non-renal losses (e.g. vomiting, diarrhoea, burns)
**therefore the point about urine sodium <20 being the most reliable indicator of hypovolaemic hyponatramiea is only in the case of extra-renal losses**
urinary sodium levels in hypervolaemic causes of hyponatraemia
- Cardiac failure: Urine Na is low
- Cirrhosis: Urine Na is low
- *- Renal failure: Urine Na is high (bc it’s not able to reabsorb sodium)**
**Karim’s path book: urine osmolality>20 mmol/L suggests renal cause**
**confirm whether it’s urine sodium or urine osmolality**
urinary sodium levels in euvolaemic causes of hyponatraemia
- Hypothyroidism: urine Na is low
- Adrenal insufficiency: urine Na is high
**- SIADH: high urine sodium**
Causes of SIADH
- CNS: subdural haematoma, subarachnoid haemorrhage, trauma, cavernous sinus thrombosis
- lung: lung cancer, pneumoniae, PE, pneumothorax
- drugs: (SSRI, sodium Valproate, TCAs, PPI, carbamazepine)
- Tumours
- Surgery (make excess ADH post-operatively)
**KM book: it’s pneumonia in the context of lung cancer rather than pneumonia itself**
what is pseudohyponatraemia
excess protein and lipids leads to apparent hyponatraemia but there is NORMAL OSMOLALITY
seen in myeloma
biochemical markers for real hyponatraemia
o LOW serum osmolality
o HIGH urine osmolality- making excess ADH so retaining water (so concentrated urine)
biochemical markers for SIADH
o LOW plasma osmolality
o HIGH urine osmolality
Investigations Ordered in Euvolaemic Hyponatraemia
TFTs- hypothyrodism
short Synacthen test- adrenal insufficiency
plasma + urine osmolality (low plasma + high urine) - SIADH
Diagnosis of SIADH
- No hypovolaemia
- No hypothyroidism
- No adrenal insufficiency
- REDUCED plasma osmolality
- INCREASED urine osmolality (>100)
KM book:
1) 2 low in the blood: low sodium and low osmolality
2) 2 high in the urine: urine sodium >20, urine osmolality high
3) 3 exclusions: no renal/adrenal/thyroid/cardiac disease, no hypovolaemia, no contributing drugs!!
**don’t forget the drugs**
Management of HYPOvolaemic Hyponatraemia
- 0.9% NaCL volume replacement
what is main concern about giving fluids to manage HYPOvolaemic Hyponatraemia
if Na raised too rapidly: cerebral pontine myelinolysis
shrinkage of cells = BBB disrupted = inflammatory cells go into brain:
- quadriplegia
- dysarthria
- dysphagia
- seizures
- coma + death
how quickly should Na be increased in management of hyponatraemia
Serum Na must NOT be corrected > 8-10mmol/L per 24 hours
should you give NaCl in SIADH
Do NOT GIVE NaCl in SIADH:
the hyponatraemia will get worse- fluid overload
can lead to cerebral oedema and death
Management of HYPERvolaemic Hyponatraemia
fluid restriction and treat underlying cause
**how does this work: essentially when you fluid restrict someone, over time they naturally start to lose water through other sources like sweating and respiration, eventually normalising fluid status and sodium concentration**
Management of EUvolaemic Hyponatraemia
fluid restriction and treat underlying cause
**Same principle: essentially when you fluid restrict someone, over time they naturally start to lose water through other sources like sweating and respiration, eventually normalising fluid status and sodium concentration**
how should you manage severe Hyponatraemia + how does it present
- Reduced GCS
- Seizures
- Seek expert help (treat with HYPERTONIC 3% saline)
if they do not have a reduced GCS and are not fitting, do NOT think about giving this
Drugs used to treat SIADH
o Demeclocycline: Monitor U&Es as risk of nephrotoxicity
o Tolvaptan: V2 receptor antagonist
- DEFINITION of Hypernatraemia
Serum [Na] > 145mmol/L
Causes of Hypernatraemia
- Unreplaced water loss:
o GI losses, sweat losses
o Renal losses: osmotic diuresis, reduced ADH release/ action (Diabetes Insipidus) - Patient cannot control water intake: people who cannot drink water e.g. children/elderly
**NB: GI losses can cause both hypntaramiea or hypernatramiea depending on whether the patient is able to drink to correct the fluid loss**
Investigations for suspected DI
- Serum glucose (exclude DM)
- Serum K+ (exclude hypoK)
- Serum Ca (exclude hyperCa)
- Plasma and urine osmolality
- Water deprivation test
main ones: plasma and urine osmolality + water deprivation test
Treating Hypernatraemia
- Fluid replacement with 5% dextrose
- treat underlying cause
how do you treat hypovolaemia AND hypernatremia
give normal saline to correct the volume depletion but then to correct the hypernatremia, you also give 5% dextrose.
**and then need to do serial sodium measurements**
- 70 y/o man
- 3-day history of diarrhoea
- Altered mental status
- Dry mucus membranes
- Serum Na+ is 168mmol/L
what is the management :
hypovolaemia AND hypernatremia:
- Correct water deficit – 5% dextrose
- Correct EC fluid volume depletion – 0.9% saline
- Serial Na+ measurements – every 4-6 hours
What are the effects of Diabetes mellitus on serum Na?
Variable effect on serum Na depending on the degree:
Hyperglycaemia: draws water out of the cells into ECF = hyponatraemia
Osmotic diuresis in uncontrolled diabetes: hypernatraemia due to renal fluid loss
biochemical markers for diabetes insipidus
HIGH plasma osmolality and LOW urine osmolality
Summary of assessment of hyponatraemia
If a patient is on diuretics, how does that affect volume status assessment?
need to stop their diuretics before measuring as this will affect their urine sodium measurement (it would be high)
is sodium predominantly an itracellular or extracellular cation?
Largely an extracellular cation, maintained by active pumping from ICF–> ECF
ECF fluid is directly dependent on Na_
What is the first step when you detect hyponatramiea in a patient?
establish whether true hyponatrameia by checking serum osmolality
a) low: true hypontaramiea
b) normal: spurious, drip arm sample, pseudohyponatramiea (hyperlipidaemia/paraproteinaemia)
- the lab detects the lipids and paraproteins to be part of water so sodium appears diluted and osmolality will be normal
c) high: glucose/mannitor infusion - these osmotically active substances draw water out of cells which dilutes down the sodium
flowchart summarising approach to hyponatramiea
Why could you get hypontaramiea post surgery?
1) overhydration with hypotonic IV fluids
2) transient increase in ADH due to the stress of the surgery
Clinical features of diabetes insipidus
Hypernatraemia (lethargy, thirst, irritability, confusion, coma, fits)
• Clinically euvolaemic
• Polyuria and polydipsia
• Urine: plasma osmolality is <2
(Urine is dilute despite concentrated plasma)
Types of diabetes inspidius
Distinguishing between diff types of diabetees inspidus and primary polydipsia
**rmb the osmolality needs to rise to >600*!!!!!
just because it rises slightly does not mean it is cranial DI
Osmolality vs osmolarity
OsmolaLity is a measure of all the particles in a solution and is measured in mmol/kg.
OsmolaRity is an alternative measure of the particles in solution and has the units mmol/L. OsmolaRity is calculated using the formula below:
Osmolarity = 2(Na + K ) + urea + glucose
You may notice we do not need to know the concentration of negative ions in order to calculate osmolarity. The concentration of negative ions should equal the concentration of positive ions. Therefore we simply multiply the positive ions by 2.
OsmolaLity and OsmolaRity should roughly equal. If they do not this is called the Osmolar gap.
You may ask why we have two different but similar terms. OsmolaRity can be easily calculated from the concentration of electrolytes, however, because it is measured per 1 Litre of solvent it can vary with temperature. OsmolaLity requires measuring in a lab using an osmometer, but does not vary with temperature as it is measured per 1 Kilogram of solvent, and is therefore the preferred term for biological systems.
Does osmometer measure osmolality or osmolarity?
Osmolality
units: mmol/kg
Is the calculated version osmolarlity or osmolality?
osmolarity
mmol/L
As a generla rule in SIADH how does the urine and plasma osmolality compare?
urine osmolality>plasma osmolality
primary polydipsia
low plasma osmolality
low urine osmolality
Which drugs cause SIADH?
SSRI, sodium Valproate, TCAs, PPI, carbamazepine
Depression: SSRI, TCAs
AED: sodium valproiate and carbamazapine
Other: PPI
what is cerebral salt wasting syndrome?
head injury leads to natriuresis –> sodium and water loss in the kdienys–> depletes intravascular volume–> stimulates release fo ADH to increase water retention
**primary problem is the salt loss from the kidenys rather than ADH secretion; ADH secretion is secondary**
