Pedia News

Hyponatraemia and SIADH

Hyponatraemia and SIADH
Hyponatraemia is co m proximately 30% of patients in hospital. It is classified as mild (>130 mmol/L), moderate (125–129 mmol/L) or severe (<125 mmol/L), according to either the degree of biochemical disturbance or the clinical state of the patient. The rate of change of sodium is more important than the absolute sodium value so patients with chronic hyponatraemia can be asymptomatic, while patients with a sudden drop can be very unwell. Early symptoms of hyponatraemia are headache, nausea, vomiting and general malaise. Later signs are confusion, agitation and drowsiness. Acute severe hyponatraemia leads to seizures, respiratory depression, coma and can result in death.

Making an accurate diagnosis of hyponatraemia requires full clinical assessment and a systematic approach. Drug history and hydration status are particularly important. Thiazide diuretics are a common cause of hyponatraemia and should be stopped if possible. Biochemical investigations include serum osmolality, urine osmolality, urine sodium, thyroid function and an assessment of cortisol reserve (09.00 cortisol or Synacthen test). It is not possible to make an accurate diagnosis without all of these investigations (Figure 8.2).
Diagnostic approach
In acute severe hyponatraemia with neurological compromise, hypertonic saline should be considered whatever the cause. This is a senior decision and should only be carried out under close supervision. In mild or moderate hyponatraemia, the diagnostic algorithm should be followed (Figure 8.2).
Serum and urine osmolality
Confirmation of low serum osmolality is important to exclude non-hypo-osmolar hyponatraemia (e.g. hyperglycaemia). Once hypotonic hyponatraemia has been confirmed, urine osmolality should be checked. A low urine osmolality (<100 mosmol/kg) suggests primary polydipsia or inappropriate administration of IV fluids. If urine osmolality is >100 mosmol/kg, urine sodium will guide the differential diagnosis.
Urine sodium
A low urine sodium (<30 mmol/L) suggests a low effective arterial volume. This is seen either resulting from true volume depletion (e.g. gastrointestinal salt loss), or when patients are clinically overloaded but have intravascular depletion (e.g. congestive cardiac failure, cirrhosis or nephrotic syndrome).
If urine sodium is >30 mmol/L and the patient is euvolaemic, syndrome of inappropriate ADH (SIADH) should be considered, although ACTH deficiency must be excluded. If urine sodium is >30 mmol/L and patients are hypovolaemic, Addison’s disease, renal and cerebral salt-wasting, or a history of vomiting should be considered – vomiting causes loss of hydrogen ions and a metabolic alkalosis, which is corrected by the renal excretion of sodium bicarbonate.
Severe hypothyroidism can cause hyponatraemia, although the mechanism is unclear.
Cause-specific treatment leads to biochemical correction. Appropriate fluid replacement in patients with hypovolaemic hyponatraemia with normal saline typically leads to improvement. In patients with hypervolaemic hyponatraemia, specialist treatment of cirrhosis, nephrotic syndrome or congestive cardiac failure is indicated.

Syndrome of inappropriate ADH
SIADH has many causes (Table 8.1). It is characterised by euvolaemic hypo-osmolar hyponatraemia in the context of low serum osmolality (<275 mosmol/kg), urine osmolality >100 mosmol/kg and urine sodium >30 mmol/L. SIADH can only be diagnosed after the exclusion of hypothyroidism, total salt depletion and ACTH deficiency.
ACTH deficiency appears identical to SIADH because it causes reduced excretion of free water, because cortisol deficiency leads to increased vasopressin activity. This is different from hyponatraemia caused by mineralocorticoid deficiency in Addison’s disease.
SIADH can be caused by underlying malignancy, most commonly lung cancer. Other respiratory and CNS pathology can also cause SIADH (Table 8.1). Many drugs can lead to SIADH, particularly anticonvulsants. If no cause for SIADH is found, cross-sectional imaging or bowel investigation may be necessary to search for an underlying malignancy. Idiopathic SIADH is a diagnosis of exclusion.
Reversal or treatment of the cause of SIADH and fluid restriction are the key aspects of management. Strict fluid restriction (1–1.5 L/day) is poorly tolerated and difficult to achieve. Drug treatment of SIADH includes demeclocycline and ADH antagonists. Demeclocycline reduces renal response to ADH but its use is limited by side effects and unpredictable pharmacokinetics. ADH antagonists (vaptans) directly block ADH action and are of use in specific clinical situations.
Acute severe hyponatraemia
Patients with acute severe hyponatraemia and neurological compromise require urgent management and intensive monitoring (Figure 8.1). In life-threatening situations when ts are unconscious or fitting, hypertonic (3%) saline can be considered.