Hyponatremia is commonly defined as a serum sodium concentration below 130 mmol/L.
Defined as a serum Na+ <130mmo/L
It affects 1% of hospital in patients (on call book), 15% (BMJ)
Most cases require no treatment.
Classification
According to serum ADH levels:
True volume depletion – gastrointestinal losses (i.e vomiting or diarrhea) or renal losses (i.e thiazides)
Decreased tissue perfusion (also called effective arterial volume depletion) due to reduced cardiac output in heart failure or to systemic vasodilation in cirrhosis
A primary (i.e not hypovolemic) increase in ADH release in the syndrome of inappropriate ADH secretion (SIADH)
According to volume status:
Hypovolemia
Normovolemia
Hypervolemia
Remember Syndrome of Inappropriate ADH (SIADH) is inappropriate secretion of ADH resulting in increased ADH levels in serum and increase ADH activity.
Hyponatreamia with high urinary Na+ Indicates inappropriate renal wasting of sodium (rather than retention, which should occur in hyponaturaemia) – Low urine osmolality.
Hypovolaemia
Diuretic excess (increase in water and sodium excretion, ADH kicks in > increase water retention).
Vomiting, NG suction (loss of acid -> increase pH -> kidneys compensate to excrete HCO- with Na+ -> more Na excretion by kidneys)
Hyponaturaemia with low urinary Na+ indicates appropriate renal conservation of sodium (High Urine osmolality)
Hypovolaemia
Diarrhoea (more bicarb excrete in faeces with Na+ kidneys retain Na).
Sweating, burns, pancreatitis (water and sodium loss – renal system retains more water and sodium – decrease Na excretion from Kidneys. ADH increase more water retention).
Euvolaemia
Hypotonic post-op fluids (water moves into RBC)
Elderly patients with poor diet (tea and toast diet)
Large volume binge beer drinking
Hypervolaemia (excess water + sodium in ECF space – reduce Na in blood and urine)
CCF
Cirrhosis of liver
Nephrotic syndrome
Hypoalbuminaemia
Remember Increasing sodium to quick can lead to central pontine myelonosis
Rapidly correcting hyponatraemia may produce permanent central nervous system injury, due to osmotic demyelination.
Patients with chronic hyponatraemia (ie known duration more than 48 hours) are particularly at risk.
Clinical manifestations typically delayed for 2-6 days.
Symptoms include dysarthria, dysphagia, paraparesis or quadriparesis, behavioural disturbances, movement disorders, seizures, lethargy, confusion, disorientation, obtundation, and coma. Severely affected patients may become “locked in”; they are awake but are unable to move or verbally communicate
Discussion