Table 1.

Major problems and risks and hierarchy of interventions need in the patient

Major problem and major risks	Hierarchy main features of interventions	Management and limits
Hyponatraemia	First, at the same time of potassium repletion.	The most widely used formulae employed in urinary assessment (Na, osmolarity or both), which are not applicable to anuric patients and are often of limited value in patients with chronic renal damage, as they presuppose that the kidneys have maintained their concentration ability, frequently lost in interstitial nephropathies, such as those frequently encountered in eating disorders and diuretic abuse.
Relative increase in water: cerebral oedema		Very slow rate indicated (8–20 mEq/day), slower in nonsymptomatic patients or in patients with chronic disorders.
		The effect of volume repletion on electrolyte levels in a presumably chronic hypovolaemic state is difficult to predict.
Rapid correction: osmotic demyelination		The laboratory errors for sodium reach 5% at low sodium levels, thus rendering management guided by serial sodium levels quite difficult.
Hypokalaemia	First, together with very slow sodium correction.	No indications for the velocity of correction reported.
		Unpredictable effect of volume repletion on potassium levels.
Cardiac arrhythmia; peripheral paralysis		Monitoring via EKG changes. There is a practical limit to the use of high potassium concentration when the correction starts on a peripheral vein for phlebitis and thrombosis. A central venous catheter is of great use, but often not immediately available in the emergency room.
Acidosis	Last, after potassium correction.	The presence of acidosis points to the presence of chronic kidney disease (in the absence of recent diarrhoea), as alkalosis is more commonly associated with diuretic use and volume contraction; acidosis should be corrected slowly and only after potassium correction with normalization of the EKG alterations.
Not life-threatening; impairment of kidney function		While there are signs of rhabdomyolysis and alkalinization of the urine is effective for improving excretion of toxic metabolites, the risks of hypokalaemia clearly overcome those of not correcting a potential factor for acute kidney failure.
Volume depletion	Slow correction, with intravenous isotonic saline; the low sodium level suggests that water is still in excess as compared with sodium.	The patient is anuric; diuretics are contraindicated in the case of volume and potassium depletions, even if they are occasionally used in hyponatraemic patients, on the account of the relative excess of water with respect to sodium.
Acute cardiovascular collapse, in particular in combination with severe hypokalaemia		The entity of volume depletion is difficult to assess, as only clinical parameters are available, in the wait for central vein catheterization, which may help in guiding infusion rate, based upon central venous pressure.
		The urine output is the clue for tailoring interventions, for the risk of a relatively rapid shift between and hypovolaemic the hypervolaemic states.
Renal failure	Postpone dialysis, when needed, at least for partial sodium correction.	Dialysis may trigger a too rapid correction of electrolytes, with an increased risk for central pontine demyelinization; dialysis with hypotonic and isotonic solutions has been performed occasionally, but the management is still based on empiric and scattered experiences.
No immediate threats, as the patient is hypovolaemic.	Careful volume management
Tetraparesis	Immediate need for intubation.	The need for intubation and sedation impairs basing or tailoring the clinical management upon symptoms of hyponatraemia (such as nausea, asthaenia and confusion).
Respiratory failure