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Hyponatraemia

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Hyponatraemia: A sudden drop in serum sodium (Na) can cause cerebral oedema, resulting in cellular swelling and dysfunction. In severe cases, this may lead to brain herniation and lasting neurological injury. A gradual decline in Na, however, is usually better tolerated. The general recommendation is to raise serum sodium by less than 12 mmol/L per day, correcting over 2–3 days if necessary to reduce the risk of complications.

Comatose Management Summary for Severe Hyponatraemia (Na < 115 mmol/L)
Airway, Breathing, Circulation (ABC): Provide immediate resuscitation if the patient is comatose or seizing (Na often <115 mmol/L). Exclude Opiate Overdose & Hypoglycaemia: Consider glucose and naloxone. Escalate to HDU/ITU as needed. Investigations: Obtain IV access; check cortisol, glucose, urine/serum Na, thyroid function tests (TFTs). Volume Status: Determine if hyponatraemia is due to water overload or sodium depletion. History Review: Assess drug use, fluid overload, and possible SIADH. Neurological Assessment: If Glasgow Coma Scale (GCS) is low, consider CT to exclude subarachnoid (SAH), subdural (SDH), intracerebral (ICH) haemorrhage, tumour, pituitary apoplexy, or CNS infection. Hypovolaemic Hyponatraemia: Give 0.5–1 L of IV normal saline; reassess clinical and laboratory parameters. Euvolaemic Hyponatraemia (e.g., SIADH) with Seizures/Coma: Restrict fluids to ~1 L/day. In urgent cases, a 150 ml bolus of 3% hypertonic saline over 15–30 mins can be considered after senior advice is taken. Raise Na by ~6-10 mmol/L per day initially to improve neurological status. Consider adding Demeclocycline or Tolvaptan for persistent SIADH. Monitor serum Na every 2–4 hours to prevent overly rapid changes. Rate of Correction: Do not exceed 12 mmol/L per 24 hours to reduce neurological risks (e.g. Central Pontine Myelinosis). Early Senior Involvement: Managing severe hyponatraemia with CNS symptoms can be complex—seek specialist input promptly.

Comatose Management Summary for Severe Hyponatraemia (Na < 115 mmol/L)

Airway, Breathing, Circulation (ABC): Provide immediate resuscitation if the patient is comatose or seizing (Na often <115 mmol/L).
Exclude Opiate Overdose & Hypoglycaemia: Consider glucose and naloxone. Escalate to HDU/ITU as needed.
Investigations: Obtain IV access; check cortisol, glucose, urine/serum Na, thyroid function tests (TFTs).
Volume Status: Determine if hyponatraemia is due to water overload or sodium depletion.
History Review: Assess drug use, fluid overload, and possible SIADH.
Neurological Assessment: If Glasgow Coma Scale (GCS) is low, consider CT to exclude subarachnoid (SAH), subdural (SDH), intracerebral (ICH) haemorrhage, tumour, pituitary apoplexy, or CNS infection.
Hypovolaemic Hyponatraemia: Give 0.5–1 L of IV normal saline; reassess clinical and laboratory parameters.
Euvolaemic Hyponatraemia (e.g., SIADH) with Seizures/Coma:
- Restrict fluids to ~1 L/day. In urgent cases, a 150 ml bolus of 3% hypertonic saline over 15–30 mins can be considered after senior advice is taken.
- Raise Na by ~6-10 mmol/L per day initially to improve neurological status.
- Consider adding Demeclocycline or Tolvaptan for persistent SIADH.
- Monitor serum Na every 2–4 hours to prevent overly rapid changes.
Rate of Correction: Do not exceed 12 mmol/L per 24 hours to reduce neurological risks (e.g. Central Pontine Myelinosis).
Early Senior Involvement: Managing severe hyponatraemia with CNS symptoms can be complex—seek specialist input promptly.

Physiology of Hyponatraemia

Low sodium normally suppresses ADH release, increasing free water excretion.
Inappropriate ADH secretion (SIADH) leads to water retention and elevated urine osmolality (>100 mOsm/kg).
Hypovolaemia triggers ADH, thirst, and aldosterone-mediated sodium reabsorption, typically lowering urinary Na.
Hyponatraemia and low serum osmolality permit water to move intracellularly, risking cerebral oedema.

Clinical Evaluation: Classify volume status as:

Examine drug history, fluid input/output charts, and assess hydration status.
Hypovolaemic: Dehydrated appearance, reduced skin turgor, hypotension, tachycardia, dry mucous membranes. Causes include GI losses, Addison’s disease, salt-wasting nephropathies.
Euvolaemic: No peripheral oedema or fluid overload signs; SIADH is common in this category.
Hypervolaemic: Oedema, ascites, or features of heart, renal, or liver failure.

Types and Causes of Hyponatraemia

Hypovolaemic: Vomiting, diarrhoea, diuretics, cerebral salt wasting, Addison’s, burns, salt-losing nephropathy.
Euvolaemic: SIADH, medications (opiates, NSAIDs, SSRIs), post-operative states, psychogenic polydipsia. Post Op causes are excessive use of 5% dextrose (free water retention). Post-surgical ADH release due to pain or stress. Post-TURP syndrome from irrigation fluid absorption.
Hypervolaemic: Heart failure, liver cirrhosis, renal failure, iatrogenic (excess hypotonic fluids), post-TURP syndrome.

Medical Causes of Hyponatraemia

Diuretics (particularly thiazides), resulting in salt/water loss.
Cardiac, hepatic, or renal failure prompting fluid retention.
SIADH causing excess water absorption in the kidneys.
Pseudohyponatraemia from hyperlipidaemia or hyperproteinaemia.

Severity of Hyponatraemia

Rapid decrease or Na <120 mmol/L increases risk of symptoms.
Na 110–115 mmol/L: Headache, confusion, irritability.
Na <110 mmol/L: Seizures, coma, ataxia, tremors (medical emergency).

Investigations

U&E: Classify hyponatraemia (mild 135–130, moderate 125–129, severe <125 mmol/L).
Serum osmolality: <275 mOsm/kg in SIADH.
Urine osmolality: >100 mOsm/kg in SIADH with hypotonic plasma.
Urine Na⁺: Typically <20 mmol/L in hypovolaemia but >30 in SIADH.
TFTs & Cortisol: Assess for hypothyroidism or adrenal insufficiency.
CXR: Look for pulmonary tumours or infections causing SIADH.
CT Head: Exclude acute neurological events in severe symptoms.
Lipids/Proteins: Rule out pseudohyponatraemia.

Central Pontine Myelinosis (CPM)

CPM is a severe risk associated with overly rapid correction of chronic hyponatraemia. It leads to demyelination (often in the pons) and may cause irreversible neurological deficits. To minimize this risk, maintain a correction rate below 12 mmol/L per 24 hours.

Algorithm

Differential Diagnosis

Pseudohyponatraemia: Often due to elevated lipids or proteins. Plasma osmolality may be normal or elevated despite a low measured Na.

Management Principles

Initial Stabilization (ABC): In severe cases with CNS involvement, consider HDU/ITU admission.
Frequent monitoring of electrolytes, NEWS score, and neurological status.
Determine if hyponatraemia is hypovolaemic, euvolaemic, or hypervolaemic and manage accordingly.
Avoid Rapid Correction: Target an increase in Na of ≤12 mmol/L per 24 hours; aim to bring Na above 120 mmol/L cautiously if severe.
For Hypovolaemia, use normal saline judiciously. Reassess frequently.
In SIADH (Euvolaemia), fluid restriction (800–1000 ml/day) is first-line. In severe symptomatic hyponatraemia, use 3% saline bolus to correct ~5 mmol/L initially, then continue with fluid restriction ± Tolvaptan or Demeclocycline.
Addison’s Disease: Confirm adrenal insufficiency (short synacthen test). Treat with IV hydrocortisone.
For Post-TURP or iatrogenic causes, consider diuretics if volume overloaded.
Hypervolaemic Hyponatraemia: Restrict fluids and salt; use loop diuretics if needed.

Makindo Medical Notes

Hyponatraemia

Physiology of Hyponatraemia

Clinical Evaluation: Classify volume status as:

Types and Causes of Hyponatraemia

Medical Causes of Hyponatraemia

Severity of Hyponatraemia

Investigations

Central Pontine Myelinosis (CPM)

Algorithm

Differential Diagnosis

Management Principles

References