70 year old female presents to ED with a 1 month history of vomiting and diarrhoea.

Metabolic alkalosis – pH 7.557 HCO3 37mmol/l

Compensation – Expected PCO2 = (0.7xHCO3) + 20 = 45.9mmHg

Lactate mildly elevated. Sodium, potassium and chloride markedly decreased, with a normal creatinine and BSL.

This patient has a metabolic alkalosis, which is adequately compensated with an expected pCO2 of 45.9 mmHg. Recall the causes of metabolic alkalosis – CLEVERPD (Contraction, Liquorice, Endocrine (Cushings, Conns, Bartters), Vomiting or NG suction, Excess alkali (antacids, dialysis), Refeeding alkalosis, Renal HCO3 retention with hypochloraemia and hypokalaemia, Post hypercapnia, Diuretics.  In this case the obvious cause for the metabolic alkalosis would be volume contraction, vomiting and renal HCO3 retention from the low potassium and chloride.

The markedly low electrolytes are related to the GI losses from the vomiting and diarrhoea as well as malabsorption from an underlying colitis.

The patient shows clinical and metabolic signs of hypovolaemic shock with a borderline BP, tachycardia, prolonged CPR and mildly elevated lactate.

To determine the cause of the low sodium in a patient one needs to consider the history and examination and 3 important lab tests – serum osmolality, urine osmolality and then urine sodium.

In all patients check the serum osmolality. It differentiates between true hyponatraemia and pseudohyponatraemia. If it is >280mOsm/kg it is due to hyperlipidaemia, hyperpronteinemia or the presence of osmotically active substances -elevated glucose or mannitol.  If serum osmolality is < 280 mOsm/kg – true hyponatraemia

If the patient is hypovolaemic – urine sodium will further differentiate the patient – urine Na <20mmol/l is due to vomiting and diarrhoea. Urine sodium >20mmol/l is due to diuretics, Addisons and salt losing nephritis.

If the patent is fluid overloaded the causes include cirrhosis, CCF and nephrosis

If the patient is euvolaemic with urine Na >20mmol/l the causes include hypothyroidism, drugs, post surgery, psychogenic polydipsia. If Na<20mmol/l causes include SIADH, drugs renal failure.

A urine osmolality <100mOsm/kg indicates excessive water intake eg psychogenic polydispsia

Treatment of hyponatraemia is based on whether it is acute or chronic and if the patient has severe signs and symptoms.

For severe hyponatraemia with severe symptoms eg seizures

• 150  ml of 3% hypertonic saline IV over 20  min. Recheck and repeat the infusion until there is a rise of sodium of 5mmol/l or symptoms improve

For patients with acute hyponatraemia – start diagnostic work up, stop offending drugs and fluids and re check sodium and treat according to underlying cause

For patients with chronic hyponatraemia  – treatment is directed at underlying cause.

In the above patient who has hypovolaemic hyponatraemia – Restore extracellular volume with an IV infusion of 0.9% saline at 0.5–1.0 ml/kg/h. In cases of hemodynamic instability, the need for rapid fluid resuscitation overrides the risk of an overly rapid increase in serum sodium concentration. Once the extracellular volume is replaced, replace sodium at a rate of 0.5mmol/hr. Increase sodium by 10mmol/l over the first 24 hours and 8mmol/l in the next 24 hours, until a sodium level of 130mmol/l.