Abstract
Disturbances in sodium concentration are common in the critically ill patient and associated with increased mortality. The key principle in treatment and prevention is that plasma [Na+] (P-[Na+]) is determined by external water and cation balances. P-[Na+] determines plasma tonicity. An important exception is hyperglycaemia, where P-[Na+] may be reduced despite plasma hypertonicity. The patient is first treated to secure airway, breathing and circulation to diminish secondary organ damage. Symptoms are critical when handling a patient with hyponatraemia. Severe symptoms are treated with 2 ml/kg 3% NaCl bolus infusions irrespective of the supposed duration of hyponatraemia. The goal is to reduce cerebral symptoms. The bolus therapy ensures an immediate and controllable rise in P-[Na+]. A maximum of three boluses are given (increases P-[Na+] about 6 mmol/l). In all patients with hyponatraemia, correction above 10 mmol/l/day must be avoided to reduce the risk of osmotic demyelination. Practical measures for handling a rapid rise in P-[Na+] are discussed. The risk of overcorrection is associated with the mechanisms that cause hyponatraemia. Traditional classifications according to volume status are notoriously difficult to handle in clinical practice. Moreover, multiple combined mechanisms are common. More than one mechanism must therefore be considered for safe and lasting correction. Hypernatraemia is less common than hyponatraemia, but implies that the patient is more ill and has a worse prognosis. A practical approach includes treatment of the underlying diseases and restoration of the distorted water and salt balances. Multiple combined mechanisms are common and must be searched for. Importantly, hypernatraemia is not only a matter of water deficit, and treatment of the critically ill patient with an accumulated fluid balance of 20 litres and corresponding weight gain should not comprise more water, but measures to invoke a negative cation balance. Reduction of hypernatraemia/hypertonicity is critical, but should not exceed 12 mmol/l/day in order to reduce the risk of rebounding brain oedema.
Highlights
Hyponatraemia and hypernatraemia are frequent in patients admitted to the ICU and may even be acquired during their stay [1,2,3,4,5,6,7,8]
One bolus of 2 ml/kg 3% NaCl results in an immediate, controllable rise in P-[Na+] of about 2 mmol/l
The key principle in treatment and prevention is that P-[Na+] is determined by external water and cation balances
Summary
Hyponatraemia and hypernatraemia are frequent in patients admitted to the ICU and may even be acquired during their stay [1,2,3,4,5,6,7,8]. A reduction in the glomerular filtration rate with increasing age, various drugs (Table 2) and various disease states (for example, reduced effective circulating volume) will render the patient more vulnerable to water ingestion Treatment should address these mechanisms: reduce water intake (avoid hypotonic fluids), improve nutrition and restore kidney function. In the critically ill patient, the mechanisms of inappropriate vasopressin secretion and thirst are heterogeneous This may be due to various drugs (Table 2), malignant disease, central nervous system disorders (infection, bleeding, thrombosis, spaceoccupying disorders, psychosis and generalised disorders), pulmonary disorders (infection, asthma, respirator treatment) or other causes (general anaesthesia, postoperative nausea, pain and stress) [78,86]. Other hyponatraemia mechanisms are likely to co-exist in the critically ill patient (for example, thiazide therapy, low solute intake, renal impairment), and it is important to determine and correct these causes.
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