Chempath - Sodium and Fluid Balance Flashcards
% of body that is water
60%
Intracellular:extracellular fluid ratio
2:1
Components of ECF
Intravascular, interstitial (largest components), transcellular (within epithelial lined spaces e.g. CSF, joint fluid, urine etc)
ECF solute components in comparison to ICF
More Na+ and Cl-
Less K+
Think of cells as primitive organisms that used to be in the sea –> need salty water to survive
Osmolality vs osmolarity
Osmolality = total number of particles in solution - measured with an osmometer, units = mmol/kg. Osmolarity = calculated, units = mmol/l
Osmolarity calculation
2(Na+ + K+) + urea + glucose
Osmolar gap
Osmolality - osmolarity
Normal range for serum osmolality
275-295 mmol/kg
Sodium normal range
135-145 mol/l
Hyponatraemia =
excess extracellular water relative to Na+
Hyponatraemia - Rx
Treat underlying cause, not the hyponatraemia (unless severe (<125mmol/l)) AND symptomatic (chronic hyponatraemias may be asymptomatic). More dangerous to correct too quickly –> central pontine myelinolysis
Hyponatraemia - Symptoms
Nausea and vomiting (<134)
Confusion (<131)
Seizures, non-cariogenic pulmonary oedema (<125)
Coma (<117) and eventual death
Hormone that controls water balance
ADH (vasopressin) - acts on V2 receptors to insert aquaporin 2 into collecting ducts to increase water reabsorption
Also - V1 receptors:
Vascular smooth muscle
Vasoconstriction (higher concentrations)
Alternative name ‘vasopressin’
2 main stimuli for ADH secretion
Serum osmolality (mediated by hypothalamic osmoreceptors). Increase in osmolality –> increased thirst and ADH secretion.
Blood volume/pressure (mediated by baroreceptors in carotids, atria, aorta). Decrease in BP –> increase in ADH
Increased ADH –> increased water reabsorption –> relative hyponatraemia.
1st step in assessing hyponatraemic patient
Assessment of fluid status
Clinical signs of hypovolaemia
Tachycardia Postural hypotension Dry mucous membranes Reduced skin turgor Confusion/drowsiness Reduced urine output Low urine Na+ (<20) --> kidneys try to hold onto the sodium to hols onto the water
Clinical signs of hypervolaemia
Raised JVP
Bibasal crackles (on chest examination)
Peripheral oedema
Causes of hypovolaemia
Gastro and renal
Diarrhoea
Vomiting
Diuretics - especially thiazides
Salt losing nephropathy
Causes of euvolaemia
Endo
Hypothyroidism
Adrenal insufficiency
SIADH
Causes of hypervolaemia
“Three Failures”
Heart failure –> reduced CO –> reduced BP –> increased ADH secretion
Renal failure
Liver failure (cirrhosis) –> NO –> vasodilation –> reduced BP –> increased ADH secretion
Difference between hypovolaemia and dehydration
Hypovolaemia - loss of water AND salt
Dehydration - loss of water
Causes of SIADH
CNS pathology
Lung pathology
Drugs (SSRIs, TCAs, opiates, PPIs, carbamazepine)
Tumours - (small cell lung cancer, pancreatic, prostate, lymphoma)
Surgery
Pseudohyponatraemia
Excess protein/lipid may be sensed by the machine as water - SODIUM WILL APPEAR DILUTED BUT OSMOLALITY WILL BE NORMAL. e.g. in multiple myeloma
Euvolaemic hyponatraemia Ix
TFTs
Short syntACTHen test
Plasma & urine osmolality (SIADH will have low plasma & high urine osmolality)
Diagnosis of SIADH
No Hypovolaemia No Hypothyroidism No Adrenal insufficiency Reduced plasma osmolality AND Increased urine osmolality (>100)
Hypovolaemic Hyponatraemia - Rx
Volume replacement with 0.9% saline
Give 250 ml –> if sodium goes up then it was hypovolaemia, if it goes down then it was euvolaemia (can use diagnostically).
Hypervolaemic/Euvolaemic Hyponatraemia - Rx
Fluid restriction
Treat the underlying cause
Severe hyponatraemia
Reduced GCS
Seizures
Seek expert help (Treat with HYPERTONIC 3% SALINE)
Serum Na must NOT be corrected > 8-10 mmol/L in the first 24 hours
Risk of osmotic demyelination (central pontine myelionlysis)
quadriplegia, dysarthria, dysphgia, seizures, coma, death
SIADH - Rx
Demeclocycline- Reduces responsiveness of collecting tubule cells to ADH. Monitor U&Es (risk of nephrotoxicity).
Tolvaptan - V2 receptor antagonist
Hypernatraemia - Main Causes
Unreplaced water loss
Gastrointestinal losses, sweat losses
Renal losses: osmotic diuresis, reduced ADH release/action (Diabetes insipidus)
Patient cannot control water intake e.g. children, elderly
Suspected Diabetes Insipidus - Ix
Serum glucose (exclude diabetes mellitus) Serum potassium (exclude hypokalaemia) Serum calcium (exclude hypercalcaemia) Plasma & urine osmolality Water deprivation test +/- desmopressin
Hypernatraemia - Rx
Fluid replacement
Treat the underlying cause
Correct water deficit - 5% DEXTROSE
Correct extracellular fluid volume depletion- 0.9% SALINE
Serial Na+ measurements - Every 4-6 hours
Effects of diabetes mellitus on serum sodium
Variable
Hyperglycaemia draws water out of the cells leading to hyponatraemia
Osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatraemia
Types of DI
Cranial:
Lack of ADH
Causes: surgery, trauma, tumours
Rx - desmopressin
Nephrogenic:
Receptor defect - insensitivity to ADH
Causes: inherited channelopathies, lithium, demeclocycline
Rx - thiazide diuretics
Hypernataraemia - Clinical Features
Lethargy, thirst, irritability, confusion, coma, fits
