Wales Critical Care & Trauma Network (North) Management of Hyponatraemia in Intensive Care Guidelines

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1 Wales Critical Care & Trauma Network (North) Management of Hyponatraemia in Intensive Care Guidelines Author: Richard Pugh June 2015

2 Guideline for management of hyponatraemia in intensive care Background Hyponatraemia is defined by serum sodium concentration of less than 135 mmol/l, and (biochemically) profound hyponatraemia by concentration of less than 125 mmol/l. Whereas chronic hyponatraemia may be relatively asymptomatic, acute hyponatraemia is more likely to be associated with severe or moderately severe symptoms (see Table 1). Hyponatraemia is an independent predictor of hospital mortality and increased length of stay. 1 Table 1. Symptoms associated with hyponatraemia (adapted from Spasovski et al. 2 ) Severity Moderately severe Symptoms Nausea Confusion Headache Severe Vomiting Seizures Altered conscious level Cardio-respiratory distress A major challenge in the treatment of hyponatraemia is that over-rapid correction, particularly when hyponatraemia has been long-standing, carries a risk of causing neurological injury, a process known as osmotic demyelination or central pontine myelinolysis. However, the underlying principle of this guideline is that the presence of moderately severe or severe symptoms should prompt urgent therapy, whereas asymptomatic chronic hyponatraemia allows time to investigate probable aetiology and institute cause-specific treatment. Aetiology The pathophysiological processes associated with the development of hyponatraemia may be complex; however contributing factors may include: Excess water intake e.g. psychogenic polydipsia, TUR syndrome Hypovolaemia - intra-vascular hypovolaemia is associated with increased ADH (also referred to as vasopressin) secretion, which causes water retention Inappropriate water retention e.g. syndrome of inappropriate ADH secretion (SIADH, which itself has multiple potential causes), hypothyroidism, post-operative state

3 Inappropriate natriuresis (renal sodium excretion) e.g. cerebral salt-wasting (for example post- subarachnoid haemorrhage), Addison s disease, diuretic use (especially thiazides), renal failure Assessment of circulating volume and extracellular fluid status will help to differentiate aetiology (see Fig 1 below). Furthermore, patients presenting with hypovolaemia associated with hyponatraemia (which is not unusual at presentation to ICU) will have increased levels of circulating vasopressin (ADH), which acts to cause water retention. On correction of hypovolaemia (e.g. with isotonic or hypertonic saline), this stimulus for vasopressin production decreases, and large volumes of dilute urine may result. Very rapid and potentially damaging rises in serum sodium concentration (e.g. >2 mmol/hr) may result. Laboratory diagnosis: spurious hyponatraaemia, and use of urine osmolality and sodium measurement 1. In some circumstances, serum sodium concentration appears low because of presence of other osmotically active substances, e.g. high concentrations of glucose, administration of mannitol, or because of artefact, e.g. pseudohypontraemia due to high triglyceride levels, or exogenous immunoglobulins. Serum sodium concentration may be corrected for hyperglycaemia using the following formula: Corrected [Na+] = measured [Na+] x [Glucose (mmol/l)- 5.5 (mmol/l) 5.5 mmol/l 2. Noting that prior use of diuretics and/ or co-existence of renal disease will make biochemical differentiation challenging - urine osmolality and sodium concentration in the context of hyponatraemia: Urine osmolality < 100 mosm/kg implies that the kidney s ability to excrete free water is unimpaired. The likely cause will be excess water intake Urine osmolality > 100 mosm/kg and urine sodium < 30 mmol/l implies (biochemically) a low intravascular volume, which may be associated with expanded (e.g. cirrhosis) or contracted extracellular volume (e.g. GI losses) Urine osmolality > 100 mosm/kg and urine sodium > 30 mmol/l is likely to represent excessive natriuresis (e.g. diuretics, cerebral injury) or inappropriate water retention (e.g. SIADH)

4 Treatment In the presence of severe or moderately severe symptoms of hyponatraemia, treatment with 150 ml (or 2 ml/kg at extremes of normal body weight) of 2.7% hypertonic saline over 20 minutes is recommended (see Fig 1 below). This does not need to be administered via a central line; however, arterial and/ or central venous access will facilitate repeated blood sampling. This dose of hypertonic saline should be repeated every 20 minutes until a rise in serum sodium of 5 mmol/l has been achieved. If symptoms associated with hyponatraemia resolve, continued infusion of normal saline should continue at lowest appropriate rate, depending on assessment of circulating volume and maintenance requirements. Serum sodium concentrations should then be re-checked after 6 hours and 12 hours, and daily thereafter. If symptoms do not resolve (and other causes for low serum sodium should be actively investigated), hypertonic saline or normal saline should continue until symptoms improve, checking serum sodium concentration every 4 hours. The formula below may help to guide saline administration: Predicted change in serum [Na+] = infusate [Na+] serum [Na+] total body water (L) +1 where total body water may be estimated by multiplying body weight by 0.6 (non-elderly men), 0.5 (non-elderly women or elderly men) or by 0.45 (elderly women). Of note, while actively managing serum sodium concentration, increases in serum sodium concentration should be limited to: 10 mmol/l over the first 24 hours* 8 mmol/l over subsequent 24 hours A target serum concentration of no more than 130 mmol/l *This limit should be reduced to 8 mmol/l over first 24 hours in presence of risk factors for osmotic demyelination, i.e. plasma sodium concentration 105 mmol/l or less, hypokalaemia, alcoholism, malnutrition, and/ or liver disease. 3 Over-rapid correction of hyponatraemia A particular problem when resuscitation corrects hypovolaemia is that high urine output associated with a sudden drop in endogenous vasopressin may lead to rapid rises in serum sodium concentration of greater than 2 mmol/l per hour, to the extent that serum sodium concentration exceeds 10 mmol/l over first 24 hours (8 mmol/l per over first 24 hours, in patients with risk factors for osmotic demyelination, as above). In this instance:

5 Active measures (e.g. administration of saline) to increase serum sodium concentration should be discontinued Consider administering 10 ml/kg 5% dextrose over 1 hour and/ or maintenance infusion of 5% dextrose Consider administration of intravenous desmopressin 2μg iv. Some authorities would advocate co-administration of desmopressin with hypertonic or isotonic saline at the outset, when hypovolaemic hyponatraemia is thought highly likely 4. Note that in the context of renal failure requiring renal replacement therapy, sterile water may be added to or 5% dextrose substituted for replacement therapy (see link) 5. Treatment of chronic hyponatramia in absence of severe/ moderately severe symptoms Assessment of circulating volume, extracellular fluid and urine biochemistry may help to establish whether cause of chronic hyponatraemia is likely to be associated with: Expanded extracellular volume in which case fluid restriction, with or without use of diuretics, may be appropriate Euvolaemia in which case evaluating thyroid and adrenal function, review of potentially contributing medication, fluid restriction, and in the case of SIADH use of demeclocyclin or vaptan (vasopressin receptor inhibitor) therapy may be considered 6 Hypovolaemia in which case fluid resuscitation with 0.9% saline or balanced crystalloid is likely to be appropriate, with care that too rapid resuscitation does not promote diuresis to the point of excessive rise in serum sodium concentration. References 1. Tzoulis, P. et al. Multicentre study of investigation and management of inpatient hyponatraemia in the UK. Postgraduate Medical Journal 2014; 90: Spasovski G. et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Intensive Care Medicine 2014; 40: Sterns, R. Disorders of plasma sodium - causes, consequences and correction. New England Journal of Medicine 2015; 372: Tzamaloukas, A. et al. Management of severe hyponatraemia: infusion of hypertonic saline and desmopressin or infusion of vasopressin inhibitors? American Journal of the Medical Sciences 2014; 348: Ostermann, M. et al. Management of sodium disorders during continuous haemofiltration. Critical Care 2010; 14: Verbalis, J. et al. Diagnosis, evaluation and treatment of hyponatremia: expert panel recommendations. American Journal of Medicine 2013; 126: S1-S Sterns, R. et al. Management of hyponatremia in the ICU. Chest 2013; 144: 672-9

6 Fig. 1 Treatment algorithm (adapted from Spasovski ) Hyponatraemia Exclude hyperglycaemia and other causes of nonhypotonic hyponatraemia Hypotonic hyponatraemia Acute or severe symptoms? NO YES 100 mosm/kg Urine osmolality >100 mosm/kg Consider: immediate treatment with hypertonic saline Consider: primary polydipsia, low solute intake, beer potomania Urine sodium concentration 30 mmol/l > 30 mmol/l Low effective arterial volume Diuretic or kidney disease? YES NO If ECF expanded, consider: heart failure, cirrhosis, nephrotic syndrome If ECF reduced, consider: diarrhoea and vomiting, "third spacing, "diuretics Consider: diuretics, kidney disease, plus other causes If ECF reduced, consider: vomiting, primary adrenal insufficiency, renal salt wasting, cerebral salt wasting, occult diuretics If ECF normal, consider: SIADH, secondary adrenal insufficiency, hypothyroidism, occult diuretics