Endocrinology - Hyponatraemia and Hypernatraemia Flashcards
What are clinical features of hyponatraemia?
- Headache
- Confusion
- Restlessness
- Seizures
- Drowsiness/coma: associated with cerebral oedema caused by low ECF:CSF osmolality
What are the 3 big categories of hyponatraemia?
- Hypovolaemic hyponatraemia
- Euvolaemic hyponatraemia
- Hypervolaemic hyponatraemia
Hypovolaemic hyponatraemia: causes
◦ Extra-renal causes (urinary Na+ <20mmol/L): vomiting, diarrhea, haemorrhage, burns, pancreatitis
◦ Renal causes (Urinary Na+ >20 mmol/L): osmotic diuresis (eg hyperglycaemia), diuretics, adrenal insufficiency (hormones), tubulo-interstitial disease, unilateral renal artery stenosis
Hypovolaemic hyponatraemia: Rx
◦ Rx underlying cause
◦ Healthy patient: give oral electrolyte-glucose mixtures + increase salt intake with slow Na+ 60-80 mmol/day
◦ Severe vomiting/diarrhea: give 2L - 5% dextrose with 20mmol K+ in each and 1L 0.9% NaCl over 24h + measurable losses
◦ Correction of acid-base abnormalities not normally required
What can urinary Na tell you about the cause of hypovolaemic hyponatraemia?
- Normal range = 20 mmol/L
- <20 mmol/L = Na+ loss is extra-renal
- > 20mmol/L = Na+ loss is renal
What is euvolaemic hyponatraemia?
• Definition: intake of water in excess of kidney’s ability to excrete it (dilutional hyponatraemia) with no change in body Na+ but plasma osmolality is low.
Name 7 categories/causes of euvolaemic hyponatraemia
◦ Iatrogenic: overuse of 5% dextrose
◦ Post op hyponatraemia: avoid hypotonic fluids post op
◦ Abnormal ADH release: vagal neuropathy, deficiency of ACTH or glucocorticoids (Addison’s), hypokalaemia, hypothyroidism
◦ SIADH
◦ Unmeasured osmotically active substances stimulating osmotic ADH release: glucose, chronic alcohol abuse, mannitol, sick-cell syndrome
◦ Psych conditions: psychogenic polydipsia, SSRIs, TCAs
◦ Increased sensitivity to ADH: chlorpropamide, tolbutamine
Euvolaemic hyponatraemia: Ix
◦ Plasma and urine electrolytes and osmolalities
‣ Low Na, Cl, urea = Low plasma osmolality
‣ High Na = high urine osmolality (tends to be higher than plasma osmolality but not always)
◦ Cortisol levels (Addison’s disease), TFT (hypothyroidism), and drug induced water retention (eg Metoclopramide)
§◦ U+Es: K+ and Mg+ depletion potentiates ADH release (causes of diuretic induced hyponatraemia)
Euvolaemic hyponatraemia: Mx for most cases, acute onset of symptoms and chronic
◦ Most cases: fluid restriction (1000ml/day) and review of diuretic therapy + correction of Mg2+ and K+
◦ Acute onset of symptoms: hypertonic saline (3%) used in v severe patients (fits/coma) - given very slowly (no more than 70mmol/h) - cannot increase serum Na more than 18mmol/48 hours
◦ Chronic: if hyponatraemia has developed slowly - correction can occur slowly too
Euvolaemic hyponatraemia: what can occur if you try and correct serum Na+ too quickly?
What rate of correction should you aim for (all types of hyponatraemia)
*Rapid rise in extracellular osmolality: results in severe shrinking of brain cells and syndrome of central pontine myelinosis (may be fatal)
Rate of correction cannot be greater than 10mmol/24h or 18 mmol/48 hours
Hypervolaemic hyponatraemia: basic definition
-Reduced ability to excrete ‘free water’
Hypervolaemic hyponatraemia: Mx
- Fluid and salt restriction
- Try and address underlying cause although most tend to be chronic (eg HF)
Hypervolaemic hyponatraemia: causes
- Heart failure
- liver failure/hypoalbuminaemia
- oligouric kidney injury
Hypernatraemia: clinical features
-Non-specific: nausea, vomiting, fever
Hypernatraemia: causes
- ADH deficiency: central diabetes insipidus
- ADH improper response: nephrogenic diabetes insipidus
- Iatrogenic: hypertonic saline, drugs with high Na+ content (piperacillin), 8.4% NaHCO3 post cardiac arrest
- Insensitivity to ADH (nephrogenic diabetes insipidus): lithium, tetracycline, ATN, osmotic diuretics, TPN, hyperosmolar hyperglycaemic state
- Others: decreased water intake, increased water loss (skin/lungs)
